FW: [agi] Lamarck Lives!(?)
An article related to how changes in the epigenonme could affect learning and memory (the subject which started this thread a week ago) http://www.technologyreview.com/biomedicine/21801/ --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
FW: [agi] Lamarck Lives!(?)
To save you the trouble the most relevant language from the below cited article is While scientists don't yet know exactly how epigenetic regulation affects memory, the theory is that certain triggers, such as exercise, visual stimulation, or drugs, unwind DNA, allowing expression of genes involved in neural plasticity. That increase in gene expression might trigger development of new neural connections and, in turn, strengthen the neural circuits that underlie memory formation. Maybe our brains are using these epigenetic mechanisms to allow us to learn and remember things, or to provide sufficient plasticity to allow us to learn and adapt, says John Satterlee http://www.nida.nih.gov/about/organization/genetics/contacts/index.html , program director of epigenetics at the National Institute on Drug Abuse, in Bethesda, MD. We have solid evidence that HDAC inhibitors massively promote growth of dendrites and increase synaptogenesis [the creation of connections between neurons], says Tsai. The process may boost memory or allow mice to regain access to lost memories by rewiring or repairing damaged neural circuits. We believe the memory trace is still there, but the animal cannot retrieve it due to damage to neural circuits, she adds. -Original Message- From: Ed Porter [mailto:[EMAIL PROTECTED] Sent: Thursday, December 11, 2008 10:28 AM To: 'agi@v2.listbox.com' Subject: FW: [agi] Lamarck Lives!(?) An article related to how changes in the epigenonme could affect learning and memory (the subject which started this thread a week ago) http://www.technologyreview.com/biomedicine/21801/ --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
After talking to an old professor of mine, it bears mentioning that epigenetic mechanisms such as methylation and histone remodeling are not the only means of altering transcription. A long established mechanism involves phosphorylation of transcription factors in the neuron (phosphorylation is a way of chemically enabling or disabling the function of a particular enzyme). In light of that I think there is some fuzziness around the use of epigenetic here because you could conceivably consider the above phosphorylation mechanism as epigenetic - functionally speaking, the effect is the same - an increase or decrease in transcription. The only difference between that and methylation etc is transience: phosphorylation of transcription factors is less permanent then altering the DNA. He also shed some light on the effects on synapses due to epigenetic mechanisms. Ed, you were wondering how synapse-specific changes could occur in response to transcription mechanisms (which are central to the neuron). Specifically: There are 2 possible answers to that puzzle (that I am aware of); 1) evidence of mRNA and translation machinery present in dendrites at the site of synapses (see papers published by Oswald Steward or 2) activity causes a specific synapse to be 'tagged' so that newly synthesized proteins in the cell body are targeted specifically to the tagged synapses. Terren --- On Thu, 12/11/08, Ed Porter [EMAIL PROTECTED] wrote: From: Ed Porter [EMAIL PROTECTED] Subject: FW: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Thursday, December 11, 2008, 10:32 AM I To save you the trouble the most relevant language from the below cited article is “While scientists don't yet know exactly how epigenetic regulation affects memory, the theory is that certain triggers, such as exercise, visual stimulation, or drugs, unwind DNA, allowing expression of genes involved in neural plasticity. That increase in gene expression might trigger development of new neural connections and, in turn, strengthen the neural circuits that underlie memory formation. Maybe our brains are using these epigenetic mechanisms to allow us to learn and remember things, or to provide sufficient plasticity to allow us to learn and adapt, says John Satterlee, program director of epigenetics at the National Institute on Drug Abuse, in Bethesda, MD. We have solid evidence that HDAC inhibitors massively promote growth of dendrites and increase synaptogenesis [the creation of connections between neurons], says Tsai. The process may boost memory or allow mice to regain access to lost memories by rewiring or repairing damaged neural circuits. We believe the memory trace is still there, but the animal cannot retrieve it due to damage to neural circuits, she adds. ” -Original Message- From: Ed Porter [mailto:[EMAIL PROTECTED] Sent: Thursday, December 11, 2008 10:28 AM To: 'agi@v2.listbox.com' Subject: FW: [agi] Lamarck Lives!(?) An article related to how changes in the epigenonme could affect learning and memory (the subject which started this thread a week ago) http://www.technologyreview.com/biomedicine/21801/ agi | Archives | Modify Your Subscription --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
It's all a big vindication for genetic memory, that's for certain. I was comfortable with the notion of certain templates, archetypes, being handed down as aspects of brain design via natural selection, but this really clears the way for organisms' life experiences to simply be copied in some form to their offspring. DNA form! It is scary to imagine memes scribbling on your genome in this way. Food for thought! :O On 12/11/08, Terren Suydam ba...@yahoo.com wrote: After talking to an old professor of mine, it bears mentioning that epigenetic mechanisms such as methylation and histone remodeling are not the only means of altering transcription. A long established mechanism involves phosphorylation of transcription factors in the neuron (phosphorylation is a way of chemically enabling or disabling the function of a particular enzyme). In light of that I think there is some fuzziness around the use of epigenetic here because you could conceivably consider the above phosphorylation mechanism as epigenetic - functionally speaking, the effect is the same - an increase or decrease in transcription. The only difference between that and methylation etc is transience: phosphorylation of transcription factors is less permanent then altering the DNA. He also shed some light on the effects on synapses due to epigenetic mechanisms. Ed, you were wondering how synapse-specific changes could occur in response to transcription mechanisms (which are central to the neuron). Specifically: There are 2 possible answers to that puzzle (that I am aware of); 1) evidence of mRNA and translation machinery present in dendrites at the site of synapses (see papers published by Oswald Steward or 2) activity causes a specific synapse to be 'tagged' so that newly synthesized proteins in the cell body are targeted specifically to the tagged synapses. Terren --- On Thu, 12/11/08, Ed Porter ewpor...@msn.com wrote: From: Ed Porter ewpor...@msn.com Subject: FW: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Thursday, December 11, 2008, 10:32 AM I To save you the trouble the most relevant language from the below cited article is While scientists don't yet know exactly how epigenetic regulation affects memory, the theory is that certain triggers, such as exercise, visual stimulation, or drugs, unwind DNA, allowing expression of genes involved in neural plasticity. That increase in gene expression might trigger development of new neural connections and, in turn, strengthen the neural circuits that underlie memory formation. Maybe our brains are using these epigenetic mechanisms to allow us to learn and remember things, or to provide sufficient plasticity to allow us to learn and adapt, says John Satterlee, program director of epigenetics at the National Institute on Drug Abuse, in Bethesda, MD. We have solid evidence that HDAC inhibitors massively promote growth of dendrites and increase synaptogenesis [the creation of connections between neurons], says Tsai. The process may boost memory or allow mice to regain access to lost memories by rewiring or repairing damaged neural circuits. We believe the memory trace is still there, but the animal cannot retrieve it due to damage to neural circuits, she adds. -Original Message- From: Ed Porter [mailto:ewpor...@msn.com] Sent: Thursday, December 11, 2008 10:28 AM To: 'agi@v2.listbox.com' Subject: FW: [agi] Lamarck Lives!(?) An article related to how changes in the epigenonme could affect learning and memory (the subject which started this thread a week ago) http://www.technologyreview.com/biomedicine/21801/ agi | Archives | Modify Your Subscription --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
Eric Burton wrote: It's all a big vindication for genetic memory, that's for certain. I was comfortable with the notion of certain templates, archetypes, being handed down as aspects of brain design via natural selection, but this really clears the way for organisms' life experiences to simply be copied in some form to their offspring. DNA form! It is scary to imagine memes scribbling on your genome in this way. Food for thought! :O Well, no: that was not the conclusion that we came to during this thread. I think we all agreed that although we could imagine ways in which some acquired information could be passed on through the DNA, the *current* evidence does not indicate that large scale transfer of memories is happening. In effect, the recent discoveries might conceivably allow nature to hand over to the next generation a 3.5 inch floppy disk (remember those?) with some data on it, whereas the implication in what you just said was that this floppy disk could be used to transfer the contents of the Googleplex :-). Not so fast, I say. Richard Loosemore On 12/11/08, Terren Suydam ba...@yahoo.com wrote: After talking to an old professor of mine, it bears mentioning that epigenetic mechanisms such as methylation and histone remodeling are not the only means of altering transcription. A long established mechanism involves phosphorylation of transcription factors in the neuron (phosphorylation is a way of chemically enabling or disabling the function of a particular enzyme). In light of that I think there is some fuzziness around the use of epigenetic here because you could conceivably consider the above phosphorylation mechanism as epigenetic - functionally speaking, the effect is the same - an increase or decrease in transcription. The only difference between that and methylation etc is transience: phosphorylation of transcription factors is less permanent then altering the DNA. He also shed some light on the effects on synapses due to epigenetic mechanisms. Ed, you were wondering how synapse-specific changes could occur in response to transcription mechanisms (which are central to the neuron). Specifically: There are 2 possible answers to that puzzle (that I am aware of); 1) evidence of mRNA and translation machinery present in dendrites at the site of synapses (see papers published by Oswald Steward or 2) activity causes a specific synapse to be 'tagged' so that newly synthesized proteins in the cell body are targeted specifically to the tagged synapses. Terren --- On Thu, 12/11/08, Ed Porter ewpor...@msn.com wrote: From: Ed Porter ewpor...@msn.com Subject: FW: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Thursday, December 11, 2008, 10:32 AM I To save you the trouble the most relevant language from the below cited article is While scientists don't yet know exactly how epigenetic regulation affects memory, the theory is that certain triggers, such as exercise, visual stimulation, or drugs, unwind DNA, allowing expression of genes involved in neural plasticity. That increase in gene expression might trigger development of new neural connections and, in turn, strengthen the neural circuits that underlie memory formation. Maybe our brains are using these epigenetic mechanisms to allow us to learn and remember things, or to provide sufficient plasticity to allow us to learn and adapt, says John Satterlee, program director of epigenetics at the National Institute on Drug Abuse, in Bethesda, MD. We have solid evidence that HDAC inhibitors massively promote growth of dendrites and increase synaptogenesis [the creation of connections between neurons], says Tsai. The process may boost memory or allow mice to regain access to lost memories by rewiring or repairing damaged neural circuits. We believe the memory trace is still there, but the animal cannot retrieve it due to damage to neural circuits, she adds. -Original Message- From: Ed Porter [mailto:ewpor...@msn.com] Sent: Thursday, December 11, 2008 10:28 AM To: 'agi@v2.listbox.com' Subject: FW: [agi] Lamarck Lives!(?) An article related to how changes in the epigenonme could affect learning and memory (the subject which started this thread a week ago) http://www.technologyreview.com/biomedicine/21801/ agi | Archives | Modify Your Subscription --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives
Re: FW: [agi] Lamarck Lives!(?)
You can see though how genetic memory encoding opens the door to acquired phenotype changes over an organism's life, though, and those could become communicable. I think Lysenko was onto something like this. Let us hope all those Soviet farmers wouldn't have just starved! ;3 On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: It's all a big vindication for genetic memory, that's for certain. I was comfortable with the notion of certain templates, archetypes, being handed down as aspects of brain design via natural selection, but this really clears the way for organisms' life experiences to simply be copied in some form to their offspring. DNA form! No it's not. 1. There is no experimental evidence that learned memories are passed to offspring in humans or any other species. 2. If memory is encoded by DNA methylation as proposed in http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html then how is the memory encoded in 10^11 separate neurons (not to mention connectivity information) transferred to a single egg or sperm cell with less than 10^5 genes? The proposed mechanism is to activate one gene and turn off another -- 1 or 2 bits. 3. The article at http://www.technologyreview.com/biomedicine/21801/ says nothing about where memory is encoded, only that memory might be enhanced by manipulating neuron chemistry. There is nothing controversial here. It is well known that certain drugs affect learning. 4. The memory mechanism proposed in http://www.ncbi.nlm.nih.gov/pubmed/16822969?ordinalpos=14itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum is distinct from (2). It proposes protein regulation at the mRNA level near synapses (consistent with the Hebbian model) rather than DNA in the nucleus. Such changes could not make their way back to the nucleus unless there was a mechanism to chemically distinguish the tens of thousands of synapses and encode this information, along with the connectivity information (about 10^6 bits per neuron) back to the nuclear DNA. Last week I showed how learning could occur in neurons rather than synapses in randomly and sparsely connected neural networks where all of the outputs of a neuron are constrained to have identical weights. The network is trained by tuning neurons toward excitation or inhibition to reduce the output error. In general an arbitrary X to Y bit binary function with N = Y 2^X bits of complexity can be learned using about 1.5N to 2N neurons with ~ N^1/2 synapses each and ~N log N training cycles. As an example I posted a program that learns a 3 by 3 bit multiplier in about 20 minutes on a PC using 640 neurons with 36 connections each. This is slower than Hebbian learning by a factor of O(N^1/2) on sequential computers, as well as being inefficient because sparse networks cannot be simulated efficiently using typical vector processing parallel hardware or memory optimized for sequential access. However this architecture is what we actually observe in neural tissue, which nevertheless does everything in parallel. The presence of neuron-centered learning does not preclude Hebbian learning occurring at the same time (perhaps at a different rate). However, the number of neurons (10^11) is much closer to Landauer's estimate of human long term memory capacity (10^9 bits) than the number of synapses (10^15). However, I don't mean to suggest that memory in either form can be inherited. There is no biological evidence for such a thing. -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
--- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: You can see though how genetic memory encoding opens the door to acquired phenotype changes over an organism's life, though, and those could become communicable. I think Lysenko was onto something like this. Let us hope all those Soviet farmers wouldn't have just starved! ;3 No, apparently you didn't understand anything I wrote. Please explain how the memory encoded separately as one bit each in 10^11 neurons through DNA methylation (the mechanism for cell differentiation, not genetic changes) is all collected together and encoded into genetic changes in a single egg or sperm cell, and back again to the brain when the organism matures. And please explain why you think that Lysenko's work should not have been discredited. http://en.wikipedia.org/wiki/Trofim_Lysenko -- Matt Mahoney, matmaho...@yahoo.com On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: It's all a big vindication for genetic memory, that's for certain. I was comfortable with the notion of certain templates, archetypes, being handed down as aspects of brain design via natural selection, but this really clears the way for organisms' life experiences to simply be copied in some form to their offspring. DNA form! No it's not. 1. There is no experimental evidence that learned memories are passed to offspring in humans or any other species. 2. If memory is encoded by DNA methylation as proposed in http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html then how is the memory encoded in 10^11 separate neurons (not to mention connectivity information) transferred to a single egg or sperm cell with less than 10^5 genes? The proposed mechanism is to activate one gene and turn off another -- 1 or 2 bits. 3. The article at http://www.technologyreview.com/biomedicine/21801/ says nothing about where memory is encoded, only that memory might be enhanced by manipulating neuron chemistry. There is nothing controversial here. It is well known that certain drugs affect learning. 4. The memory mechanism proposed in http://www.ncbi.nlm.nih.gov/pubmed/16822969?ordinalpos=14itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum is distinct from (2). It proposes protein regulation at the mRNA level near synapses (consistent with the Hebbian model) rather than DNA in the nucleus. Such changes could not make their way back to the nucleus unless there was a mechanism to chemically distinguish the tens of thousands of synapses and encode this information, along with the connectivity information (about 10^6 bits per neuron) back to the nuclear DNA. Last week I showed how learning could occur in neurons rather than synapses in randomly and sparsely connected neural networks where all of the outputs of a neuron are constrained to have identical weights. The network is trained by tuning neurons toward excitation or inhibition to reduce the output error. In general an arbitrary X to Y bit binary function with N = Y 2^X bits of complexity can be learned using about 1.5N to 2N neurons with ~ N^1/2 synapses each and ~N log N training cycles. As an example I posted a program that learns a 3 by 3 bit multiplier in about 20 minutes on a PC using 640 neurons with 36 connections each. This is slower than Hebbian learning by a factor of O(N^1/2) on sequential computers, as well as being inefficient because sparse networks cannot be simulated efficiently using typical vector processing parallel hardware or memory optimized for sequential access. However this architecture is what we actually observe in neural tissue, which nevertheless does everything in parallel. The presence of neuron-centered learning does not preclude Hebbian learning occurring at the same time (perhaps at a different rate). However, the number of neurons (10^11) is much closer to Landauer's estimate of human long term memory capacity (10^9 bits) than the number of synapses (10^15). However, I don't mean to suggest that memory in either form can be inherited. There is no biological evidence for such a thing. -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
I don't think that each inheritor receives a full set of the original's memories. But there may have *evolved* in spite of the obvious barriers, a means of transferring primary or significant experience from one organism to another in genetic form... we can imagine such a thing given this news! On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: You can see though how genetic memory encoding opens the door to acquired phenotype changes over an organism's life, though, and those could become communicable. I think Lysenko was onto something like this. Let us hope all those Soviet farmers wouldn't have just starved! ;3 No, apparently you didn't understand anything I wrote. Please explain how the memory encoded separately as one bit each in 10^11 neurons through DNA methylation (the mechanism for cell differentiation, not genetic changes) is all collected together and encoded into genetic changes in a single egg or sperm cell, and back again to the brain when the organism matures. And please explain why you think that Lysenko's work should not have been discredited. http://en.wikipedia.org/wiki/Trofim_Lysenko -- Matt Mahoney, matmaho...@yahoo.com On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: It's all a big vindication for genetic memory, that's for certain. I was comfortable with the notion of certain templates, archetypes, being handed down as aspects of brain design via natural selection, but this really clears the way for organisms' life experiences to simply be copied in some form to their offspring. DNA form! No it's not. 1. There is no experimental evidence that learned memories are passed to offspring in humans or any other species. 2. If memory is encoded by DNA methylation as proposed in http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html then how is the memory encoded in 10^11 separate neurons (not to mention connectivity information) transferred to a single egg or sperm cell with less than 10^5 genes? The proposed mechanism is to activate one gene and turn off another -- 1 or 2 bits. 3. The article at http://www.technologyreview.com/biomedicine/21801/ says nothing about where memory is encoded, only that memory might be enhanced by manipulating neuron chemistry. There is nothing controversial here. It is well known that certain drugs affect learning. 4. The memory mechanism proposed in http://www.ncbi.nlm.nih.gov/pubmed/16822969?ordinalpos=14itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum is distinct from (2). It proposes protein regulation at the mRNA level near synapses (consistent with the Hebbian model) rather than DNA in the nucleus. Such changes could not make their way back to the nucleus unless there was a mechanism to chemically distinguish the tens of thousands of synapses and encode this information, along with the connectivity information (about 10^6 bits per neuron) back to the nuclear DNA. Last week I showed how learning could occur in neurons rather than synapses in randomly and sparsely connected neural networks where all of the outputs of a neuron are constrained to have identical weights. The network is trained by tuning neurons toward excitation or inhibition to reduce the output error. In general an arbitrary X to Y bit binary function with N = Y 2^X bits of complexity can be learned using about 1.5N to 2N neurons with ~ N^1/2 synapses each and ~N log N training cycles. As an example I posted a program that learns a 3 by 3 bit multiplier in about 20 minutes on a PC using 640 neurons with 36 connections each. This is slower than Hebbian learning by a factor of O(N^1/2) on sequential computers, as well as being inefficient because sparse networks cannot be simulated efficiently using typical vector processing parallel hardware or memory optimized for sequential access. However this architecture is what we actually observe in neural tissue, which nevertheless does everything in parallel. The presence of neuron-centered learning does not preclude Hebbian learning occurring at the same time (perhaps at a different rate). However, the number of neurons (10^11) is much closer to Landauer's estimate of human long term memory capacity (10^9 bits) than the number of synapses (10^15). However, I don't mean to suggest that memory in either form can be inherited. There is no biological evidence for such a thing. -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox:
Re: FW: [agi] Lamarck Lives!(?)
Evolution is not magic. You haven't addressed the substance of Matt's questions at all. What you're suggesting is magical unless you can talk about specific mechanisms, as Richard did last week. Richard's idea - though it is extremely unlikely and lacks empirical evidence to support it - is technically plausible. He proposed a logical chain of ideas, which can be supported and/or criticized, something you need to do if you expect to be taken seriously. There are obvious parallels here with AGI. It's very easy to succumb to magical or pseudo-explanations of intelligence. So talk specifically and technically about *mechanisms* (even if extremely unlikely) and you're not wasting anyone's time. Terren --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: From: Eric Burton brila...@gmail.com Subject: Re: FW: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Thursday, December 11, 2008, 6:33 PM I don't think that each inheritor receives a full set of the original's memories. But there may have *evolved* in spite of the obvious barriers, a means of transferring primary or significant experience from one organism to another in genetic form... we can imagine such a thing given this news! On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: You can see though how genetic memory encoding opens the door to acquired phenotype changes over an organism's life, though, and those could become communicable. I think Lysenko was onto something like this. Let us hope all those Soviet farmers wouldn't have just starved! ;3 No, apparently you didn't understand anything I wrote. Please explain how the memory encoded separately as one bit each in 10^11 neurons through DNA methylation (the mechanism for cell differentiation, not genetic changes) is all collected together and encoded into genetic changes in a single egg or sperm cell, and back again to the brain when the organism matures. And please explain why you think that Lysenko's work should not have been discredited. http://en.wikipedia.org/wiki/Trofim_Lysenko -- Matt Mahoney, matmaho...@yahoo.com On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: It's all a big vindication for genetic memory, that's for certain. I was comfortable with the notion of certain templates, archetypes, being handed down as aspects of brain design via natural selection, but this really clears the way for organisms' life experiences to simply be copied in some form to their offspring. DNA form! No it's not. 1. There is no experimental evidence that learned memories are passed to offspring in humans or any other species. 2. If memory is encoded by DNA methylation as proposed in http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html then how is the memory encoded in 10^11 separate neurons (not to mention connectivity information) transferred to a single egg or sperm cell with less than 10^5 genes? The proposed mechanism is to activate one gene and turn off another -- 1 or 2 bits. 3. The article at http://www.technologyreview.com/biomedicine/21801/ says nothing about where memory is encoded, only that memory might be enhanced by manipulating neuron chemistry. There is nothing controversial here. It is well known that certain drugs affect learning. 4. The memory mechanism proposed in http://www.ncbi.nlm.nih.gov/pubmed/16822969?ordinalpos=14itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum is distinct from (2). It proposes protein regulation at the mRNA level near synapses (consistent with the Hebbian model) rather than DNA in the nucleus. Such changes could not make their way back to the nucleus unless there was a mechanism to chemically distinguish the tens of thousands of synapses and encode this information, along with the connectivity information (about 10^6 bits per neuron) back to the nuclear DNA. Last week I showed how learning could occur in neurons rather than synapses in randomly and sparsely connected neural networks where all of the outputs of a neuron are constrained to have identical weights. The network is trained by tuning neurons toward excitation or inhibition to reduce the output error. In general an arbitrary X to Y bit binary function with N = Y 2^X bits of complexity can be learned using about 1.5N to 2N neurons with ~ N^1/2 synapses each and ~N log N training cycles. As an example I posted a program that learns a 3 by 3 bit multiplier in about 20 minutes on a PC using 640 neurons with 36 connections each. This is slower than Hebbian learning by a factor of O
Re: FW: [agi] Lamarck Lives!(?)
--- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: I don't think that each inheritor receives a full set of the original's memories. But there may have *evolved* in spite of the obvious barriers, a means of transferring primary or significant experience from one organism to another in genetic form... we can imagine such a thing given this news! Well, we could, if there was any evidence whatsoever for Lamarckian evolution, and if we thought with our reproductive organs. To me, it suggests that AGI could be implemented with a 10^4 speedup over whole brain emulation -- maybe. Is it possible to emulate a sparse neural network with 10^11 adjustable neurons and 10^15 fixed, random connections using a non-sparse neural network with 10^11 adjustable connections? -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
I don't know how you derived the value 10^4, Matt, but that seems reasonable to me. Terren, let me go back to the article and try to understand what exactly it says is happening. Certainly that's my editorial's crux On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: I don't think that each inheritor receives a full set of the original's memories. But there may have *evolved* in spite of the obvious barriers, a means of transferring primary or significant experience from one organism to another in genetic form... we can imagine such a thing given this news! Well, we could, if there was any evidence whatsoever for Lamarckian evolution, and if we thought with our reproductive organs. To me, it suggests that AGI could be implemented with a 10^4 speedup over whole brain emulation -- maybe. Is it possible to emulate a sparse neural network with 10^11 adjustable neurons and 10^15 fixed, random connections using a non-sparse neural network with 10^11 adjustable connections? -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
Ok. We think we're seeing short-term memories forming in the hippocampus and slowly turning into long-term memories in the cortex, says Miller, who presented the results last week at the Society for Neuroscience meeting in Washington DC. It certainly sounds like the genetic changes are limited to the brain itself. Perhaps there is some kind of extra DNA scratch space allotted to cranial nerve cells. I understand that psilocybin, a phosphorylated serotonin-like neurotransmitter found in fungal mycelia, may have evolved as a phosphorous bank for all the DNA needed in spore production. The structure of fungal mycelia closely approximates that of the brains found in the animal kingdom, which may have evolved from the same or some shared point. Then we see how the brain can be viewed as a qualified, indeed purpose-built DNA recombination factory! Fungal mycelia could be approaching all this from the opposite direction, doing DNA computation incidentally so as to perform short-term weather forecasts and other environmental calculations, simply because there is so much of it about for the next sporulation. A really compelling avenue for investigation The cool idea here is that the brain could be borrowing a form of cellular memory from developmental biology to use for what we think of as memory, says Marcelo Wood, who researches long-term memory at the University of California, Irvine. Yes. It is Eric B On 12/11/08, Eric Burton brila...@gmail.com wrote: I don't know how you derived the value 10^4, Matt, but that seems reasonable to me. Terren, let me go back to the article and try to understand what exactly it says is happening. Certainly that's my editorial's crux On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: I don't think that each inheritor receives a full set of the original's memories. But there may have *evolved* in spite of the obvious barriers, a means of transferring primary or significant experience from one organism to another in genetic form... we can imagine such a thing given this news! Well, we could, if there was any evidence whatsoever for Lamarckian evolution, and if we thought with our reproductive organs. To me, it suggests that AGI could be implemented with a 10^4 speedup over whole brain emulation -- maybe. Is it possible to emulate a sparse neural network with 10^11 adjustable neurons and 10^15 fixed, random connections using a non-sparse neural network with 10^11 adjustable connections? -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
That made almost no sense to me. I'm not trying to be rude here, but that sounded like the ramblings of one who doesn't have the necessary grasp of the key ideas required to speculate intelligently about these things. The fact that you once again managed to mention psilocybin does nothing to help your cause, either... and that's coming from someone who believes that psychedelics can be valuable, if used properly. Terren --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: From: Eric Burton brila...@gmail.com Subject: Re: FW: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Thursday, December 11, 2008, 9:11 PM Ok. We think we're seeing short-term memories forming in the hippocampus and slowly turning into long-term memories in the cortex, says Miller, who presented the results last week at the Society for Neuroscience meeting in Washington DC. It certainly sounds like the genetic changes are limited to the brain itself. Perhaps there is some kind of extra DNA scratch space allotted to cranial nerve cells. I understand that psilocybin, a phosphorylated serotonin-like neurotransmitter found in fungal mycelia, may have evolved as a phosphorous bank for all the DNA needed in spore production. The structure of fungal mycelia closely approximates that of the brains found in the animal kingdom, which may have evolved from the same or some shared point. Then we see how the brain can be viewed as a qualified, indeed purpose-built DNA recombination factory! Fungal mycelia could be approaching all this from the opposite direction, doing DNA computation incidentally so as to perform short-term weather forecasts and other environmental calculations, simply because there is so much of it about for the next sporulation. A really compelling avenue for investigation The cool idea here is that the brain could be borrowing a form of cellular memory from developmental biology to use for what we think of as memory, says Marcelo Wood, who researches long-term memory at the University of California, Irvine. Yes. It is Eric B On 12/11/08, Eric Burton brila...@gmail.com wrote: I don't know how you derived the value 10^4, Matt, but that seems reasonable to me. Terren, let me go back to the article and try to understand what exactly it says is happening. Certainly that's my editorial's crux On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: I don't think that each inheritor receives a full set of the original's memories. But there may have *evolved* in spite of the obvious barriers, a means of transferring primary or significant experience from one organism to another in genetic form... we can imagine such a thing given this news! Well, we could, if there was any evidence whatsoever for Lamarckian evolution, and if we thought with our reproductive organs. To me, it suggests that AGI could be implemented with a 10^4 speedup over whole brain emulation -- maybe. Is it possible to emulate a sparse neural network with 10^11 adjustable neurons and 10^15 fixed, random connections using a non-sparse neural network with 10^11 adjustable connections? -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
--- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: I don't know how you derived the value 10^4, Matt, but that seems reasonable to me. Terren, let me go back to the article and try to understand what exactly it says is happening. Certainly that's my editorial's crux A simulation of a neural network with 10^15 synapses requires 10^15 operations to update the activation levels of the neurons. If we assume 100 ms resolution, that is 10^16 operations per second. If memory is stored in neurons rather than synapses, as suggested in the original paper (see http://www.cell.com/neuron/retrieve/pii/S0896627307001420 ) then the brain has a memory capacity of at most 10^11 bits, which could be simulated by a neural network with 10^11 connections (or 10^12 operations per second). This assumes that (1) the networks are equivalent and (2) that there isn't any secondary storage in synapses in addition to neurons. The program I posted last week was intended to show (1). However (2) has not been shown. The fact that DNA methylation occurs in the cortex does not exclude the possibility of more than one memory mechanism. As a counter argument, the cortex has about 10^4 times as much storage as the hippocampus (10^4 days vs. 1 day), but is not 10^4 times larger. -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: FW: [agi] Lamarck Lives!(?)
I've actually got a pretty solid grasp on the underpinnings of this stuff, Terren. I was agreeing with you: memory formation via gene modification may be only endemic. Probably not all or the reproductive cells have their nuclei written to by every, or any, given stimulus. Yet, there are arguments from ancestral memory and morphogenic fields and stranger things to explain. What I see here is a blurring of the mechanisms of thought, memory, and genetic storage, that I think is hinted at in our evolutionary past. I could have expressed that a lot better. I apologise ;o On 12/11/08, Matt Mahoney matmaho...@yahoo.com wrote: --- On Thu, 12/11/08, Eric Burton brila...@gmail.com wrote: I don't know how you derived the value 10^4, Matt, but that seems reasonable to me. Terren, let me go back to the article and try to understand what exactly it says is happening. Certainly that's my editorial's crux A simulation of a neural network with 10^15 synapses requires 10^15 operations to update the activation levels of the neurons. If we assume 100 ms resolution, that is 10^16 operations per second. If memory is stored in neurons rather than synapses, as suggested in the original paper (see http://www.cell.com/neuron/retrieve/pii/S0896627307001420 ) then the brain has a memory capacity of at most 10^11 bits, which could be simulated by a neural network with 10^11 connections (or 10^12 operations per second). This assumes that (1) the networks are equivalent and (2) that there isn't any secondary storage in synapses in addition to neurons. The program I posted last week was intended to show (1). However (2) has not been shown. The fact that DNA methylation occurs in the cortex does not exclude the possibility of more than one memory mechanism. As a counter argument, the cortex has about 10^4 times as much storage as the hippocampus (10^4 days vs. 1 day), but is not 10^4 times larger. -- Matt Mahoney, matmaho...@yahoo.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
--- On Wed, 12/3/08, Ben Goertzel [EMAIL PROTECTED] wrote: Well, LTP is definitely real ... and I'm quite sure the scheme you describe is *not* how learning works in the brain ;-) ,,, but I'm equally sure that the full story has not yet been uncovered... I have attached a program that illustrates how memory can be stored in neurons rather than synapses. In a feed-forward configuration, each neuron is randomly connected to others further back, rather than fully connected. The network is sparse, with around n^(1/2) connections each among n neurons so that there is usually a path between each input and output going through at most one or two intermediate neurons. It also differs from a normal network in that all of the output weights of each neuron are constrained to have the same value. In other words, the activation level x[i] of the i'th neuron is given by x[i] = w[i]/(1+exp(-SUM_j x[j])) where j ranges over the input neurons for x[i]. Note that there is only one weight w[i] per neuron, rather than one per synapse. For the output neurons, w[i] = 1. For all others, the network is trained by adjusting the weights to reduce the RMS output error. This can be done in many ways. For example, you could simulate reinforcement learning by making random changes to w[i] and keeping changes that are followed by a reward computed by comparing desired and actual outputs. I used a more efficient training method, although I kept equivalence to biologically plausible models in mind. I used the following method: select one neuron x[i] at random and calculate the network outputs for w[i], w[i]+d, and w[i]-d for some large delta d like 0.5. Calculate the sum of the squares of the errors (actual - desired)^2 over all the values in the domain of the objective function (the desired behavior). If w[i]+d or w[i]-d gives a smaller total error than w[i], then make that the new weight. Otherwise replace d with d/2 and try again. When d is sufficiently small (like 0.02), then take the best weight and stop. Repeat until the errors are small enough. Neuron centered memory has the same information theoretical constraints as normal Hebbian learning. If your objective function has n bits of complexity, you need at least n neurons (rather than n synapses), because each parameter stores about 1 bit. Also, because each training session communicates about 1 bit, you need at least n sessions, actually O(n log n) to remove the last bit error assuming exponential convergence. In my program, I demonstrate training a neural network to learn a 3 by 3 bit multiplier. In general, a function with NX inputs and NY outputs has NY * 2^NX bits of complexity. For the 3x3 multiplier, NX = NY = 6 = 384 bits. In practice, you need 1.5 to 2 times as much. I used 640 neurons including 6 input and 6 outputs, and 36 random connections per neuron. Training should therefore require 640 * log(640) ~ 6000 sessions, although in practice about 15,000 were needed. The total number of operations is 15000 * 64 * 640 * 36 = 2.2 x 10^10, which took about 20 minutes on my PC. I estimate training a 4x4 multiplier would take about 40 times as long. I do not recommend using neuron-centered networks for solving problems that could be solved using Hebbian learning. This approach is slower by a factor of O(n^(1/2)), in this case 36, not to mention the difficulty of simulating sparse networks on vector processors. The purpose of this program is to show the plausibility of neuron-centered memory in the human brain. The brain would not be affected by the speed penalty because synapse operations are parallel. Furthermore, the model explains most of the discrepancy between Landauer's estimate of 10^9 bits of long term memory and 10^15 synapses. There are 10^11 neurons, a much closer number. Also, this model does not preclude Hebbian learning. Both could occur simultaneously. After all, learning is really a simple idea. The brain is adaptive. You just fiddle with knobs until you get the desired result. You don't have to understand what the knobs do. I believe you could achieve learning in sparse networks by fiddling with just about any neuron-wide parameters. -- Matt Mahoney, [EMAIL PROTECTED] --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com nn.cpp Description: Binary data
[agi] Lamarck Lives!(?)
Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Note also, http://sciencelinks.jp/j-east/article/200308/20030803A0129895.php Jean Baptiste de Lamarck (1744-1829) maintained that characteristics that were acquired during an organism's lifetime are passed on to its offspring. This theory, known as Lamarckian inheritance, was later completely discredited. However, recent progress in epigenetics research suggests it needs to be reexamined in consideration of DNA methylation. In this article, I summarize our observations, which support Lamarckian inheritance. Initial experiments indicate that (1) artificially induced demethylation of rice genomic DNA results in heritable dwarfism, and (2) cold stress induces extensive demethylation in somatic cells of the maize root. Based on these results, I propose the hypothesis that traits that are acquired during plant growth are sometimes inherited by their progeny through persistent alteration of the DNA methylation status. (author abst.) I wonder how this relates to adaptive mutagenesis http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1206667 which has been rather controversial http://www.genetics.org/cgi/content/full/165/4/2319 ben On Wed, Dec 3, 2008 at 11:11 AM, Richard Loosemore [EMAIL PROTECTED] wrote: Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com -- Ben Goertzel, PhD CEO, Novamente LLC and Biomind LLC Director of Research, SIAI [EMAIL PROTECTED] I intend to live forever, or die trying. -- Groucho Marx --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
On 12/3/2008 8:11 AM, Richard Loosemore wrote: Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Yes, but it obviously needs a lot more confirmation first. :-) Would it mean that memories (including cultural adaptations) could be passed from mother to child? No. As far as I understand it, they are proposing changes to the DNA in the neural cells only, so it wouldn't be passed on. And I would expect that the changes are specific to the neural structure of the subject, so even if you moved the changes to DNA in another subject, it wouldn't work. Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? No bets here. But they are proposing that elements are added onto the DNA, not that changes are made in arbitrary locations within the DNA, so it's not /quite/ as bad as you suggest --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
Richard, The role played by the epigenome in genetics actually does have a slightly Lamarckian tinge. Nova had a show saying that when identical twins are born their epigenomes are very similar, but that as they age their epigenomes start to differ more an more, and that certain behaviors like drinking or smoking can increase the rate at which such changes take place. What I didn't understand about the article you linked to is that it appears they are changing the epigenome to change the expression of DNA, but as far as I know DNA only appears in the nucleus (with the exception of mitochondirial DNA), and thus would appear to affect the cell as a whole, and thus not be good at differentially affecting the strengths of different synapses --- as would presumably be required for most neuronal memory --- unless the nuclear DNA had some sort of mapping to individual synapses, or unless local changes to mitochondrial DNA, near a synapse are involved. The article does not appear to shed in any light on this issue of how changes in the expression of DNA would affect learning at the synapse level, where most people think it occurs. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 11:12 AM To: agi@v2.listbox.com Subject: [agi] Lamarck Lives!(?) Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on -your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Interesting. Note, however, that it is conceivable that those other examples of plant and bacterial adaptation could be explained as situation-specific - in the sense that the particular cause of the adaptation could have worked in ways that were not generalizable to other, similar factors. So, some very specific factors could be inherited while others could never have an effect because they just don't happen to affect methylation. But if the neural results hold up, this would be a whole new ball game: a completely general mechanism for storing memories in an inheritable form. Not just [memory-for-your-first-kiss] affecting the DNA, but the whole shebang. If it turns out that this is the correct interpretation, then this is one hell of a historic moment. I must say, I am still a little skeptical, but we'll see how it plays out. Richard Loosemore Ben Goertzel wrote: Note also, http://sciencelinks.jp/j-east/article/200308/20030803A0129895.php Jean Baptiste de Lamarck (1744-1829) maintained that characteristics that were acquired during an organism's lifetime are passed on to its offspring. This theory, known as Lamarckian inheritance, was later completely discredited. However, recent progress in epigenetics research suggests it needs to be reexamined in consideration of DNA methylation. In this article, I summarize our observations, which support Lamarckian inheritance. Initial experiments indicate that (1) artificially induced demethylation of rice genomic DNA results in heritable dwarfism, and (2) cold stress induces extensive demethylation in somatic cells of the maize root. Based on these results, I propose the hypothesis that traits that are acquired during plant growth are sometimes inherited by their progeny through persistent alteration of the DNA methylation status. (author abst.) I wonder how this relates to adaptive mutagenesis http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1206667 which has been rather controversial http://www.genetics.org/cgi/content/full/165/4/2319 ben On Wed, Dec 3, 2008 at 11:11 AM, Richard Loosemore [EMAIL PROTECTED] wrote: Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Harry Chesley wrote: On 12/3/2008 8:11 AM, Richard Loosemore wrote: Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Yes, but it obviously needs a lot more confirmation first. :-) Would it mean that memories (including cultural adaptations) could be passed from mother to child? No. As far as I understand it, they are proposing changes to the DNA in the neural cells only, so it wouldn't be passed on. And I would expect that the changes are specific to the neural structure of the subject, so even if you moved the changes to DNA in another subject, it wouldn't work. You're right, of course. But if this holds up, it would not be quite so crazy to imagine a mechanism that uses junk DNA signalling to get the end caps of the genital DNA to reflect the changes. I admit, though, this is stretching it a bit ;-). As for the changes not working in another subject: yes, it would probably be the case that specific memories are encoded in an individual-specific way. But what about more general factors? What if there were some primitive types of musical understanding, say, that were common across individuals, for example? Like, a set of very primitive concepts having to do with links between sounds and finger movements? If such general factors could be passed across, a person could inherit above average musical ability because their parents had been active musicians all their lives. All this is fun to think about, but I confess I am mostly playing devil's advocate here. Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? No bets here. But they are proposing that elements are added onto the DNA, not that changes are made in arbitrary locations within the DNA, so it's not /quite/ as bad as you suggest It would be pretty embarrassing for people gearing up for scans with a limiting resolution at about the size of one neuron, though. IIRC that was the rough order of magnitude assumed in the proposal I reviewed here recently. Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? No bets here. But they are proposing that elements are added onto the DNA, not that changes are made in arbitrary locations within the DNA, so it's not /quite/ as bad as you suggest It would be pretty embarrassing for people gearing up for scans with a limiting resolution at about the size of one neuron, though. IIRC that was the rough order of magnitude assumed in the proposal I reviewed here recently. When I saw Todd Huffman give a presentation on brain imaging aimed toward WBE last year, he was showing images revealing individual proteins expressed around in the brain ... and the challenge was to infer higher-level stuff like synaptic potentiation from this lower-level protein-expression imaging data My recollection of the details is fuzzy, but anyway I'm clear that he and others in that field are working on lower-level imaging as well as neuron-level... ben g --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
2008/12/3 Richard Loosemore [EMAIL PROTECTED]: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? No. They are saying memories might be stored as changes *on* the DNA. Imagine a big long DNA molecule. It has little molecules attached to bits of it, which regulate which genes are and aren't expressed. That's how a cell knows it's a skin cell, or an eye cell or a liver cell. Apparently the same mechanism is used in neurons are part of the mechanism for laying down new memories. Would it mean that memories (including cultural adaptations) could be passed from mother to child? No, for two reasons: (1) the DNA isn't being changed. (2) even if the DNA was being changed, it isn't in the germ-line. (Incidently, my understanding is[*] that DNA in various cells in the mammalian immune system does change as the immune system evolves to cope with infectious agents; but these changes aren't passed along to the next generation.) * if there are any molecular biologists reading, feel free to correct me. -- Philip Hunt, [EMAIL PROTECTED] Please avoid sending me Word or PowerPoint attachments. See http://www.gnu.org/philosophy/no-word-attachments.html --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Hi Richard, Thanks for the link, pretty intriguing. It's important to note that the mechanism proposed is just a switch that turns specific genes off... so properly understood, it's likely that the resolution required to model this mechanism would not necessarily require modeling the entire DNA strand. It seems more likely that these methylation caps are being applied to very specific genes that produce proteins heavily implicated in the dynamics of synapse creation/destruction (or some other process related to memory). So modeling the phenomenon could very possibly be done functionally. Memories could only be passed to the child if 1) those DNA changes were also made in the germ cells (i.e. egg/sperm) and 2) the DNA changes involved resulted in a brain organization in the child that mimicked the parent's brain. (1) is very unlikely but theoretically possible; (2) is impossible for two reasons. One is, the methylation patterns proposed involve a large number of neurons, converging on a pattern of methylation; in contrast, a germ cell would only capture the methylation of a single cell (which would then be cloned in the developing fetus). Second, the hypothesized methylation patterns represent a different medium of information storage in the mature brain than what is normally considered to be the role of DNA in the developing brain. It would truly be a huge leap to suggest that the information stored via this alteration of DNA would result in that information being preserved somehow in a developing brain. There are plenty of other epigenetic phenomena to get Lamarck fans excited, but this isn't one of them. Terren --- On Wed, 12/3/08, Richard Loosemore [EMAIL PROTECTED] wrote: From: Richard Loosemore [EMAIL PROTECTED] Subject: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Wednesday, December 3, 2008, 11:11 AM Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
2008/12/3 Richard Loosemore [EMAIL PROTECTED]: Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? No bets here. But they are proposing that elements are added onto the DNA, not that changes are made in arbitrary locations within the DNA, so it's not /quite/ as bad as you suggest It would be pretty embarrassing for people gearing up for scans with a limiting resolution at about the size of one neuron, though. IIRC that was the rough order of magnitude assumed in the proposal I reviewed here recently. It might well be. It is anyway apparent that there are different mechanisms in the brain for laying down long-term memories and for short-term thinking over the order of a few seconds. -- Philip Hunt, [EMAIL PROTECTED] Please avoid sending me Word or PowerPoint attachments. See http://www.gnu.org/philosophy/no-word-attachments.html --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
Ed, That's a good point about synapses, but perhaps the methylation just affects the neuron's output, e.g., the targeted genes express proteins that only find a functional role in the axon. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Richard, The role played by the epigenome in genetics actually does have a slightly Lamarckian tinge. Nova had a show saying that when identical twins are born their epigenomes are very similar, but that as they age their epigenomes start to differ more an more, and that certain behaviors like drinking or smoking can increase the rate at which such changes take place. What I didn't understand about the article you linked to is that it appears they are changing the epigenome to change the expression of DNA, but as far as I know DNA only appears in the nucleus (with the exception of mitochondirial DNA), and thus would appear to affect the cell as a whole, and thus not be good at differentially affecting the strengths of different synapses --- as would presumably be required for most neuronal memory --- unless the nuclear DNA had some sort of mapping to individual synapses, or unless local changes to mitochondrial DNA, near a synapse are involved. The article does not appear to shed in any light on this issue of how changes in the expression of DNA would affect learning at the synapse level, where most people think it occurs. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 11:12 AM To: agi@v2.listbox.com Subject: [agi] Lamarck Lives!(?) Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on -your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Philip Hunt wrote: 2008/12/3 Richard Loosemore [EMAIL PROTECTED]: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? No. They are saying memories might be stored as changes *on* the DNA. Imagine a big long DNA molecule. It has little molecules attached to bits of it, which regulate which genes are and aren't expressed. That's how a cell knows it's a skin cell, or an eye cell or a liver cell. Apparently the same mechanism is used in neurons are part of the mechanism for laying down new memories. Yes, I know this: I appreciate the difference between tampering with the gene regulation apparatus and affecting the codons themselves, but for my money, *any* mechanism that collects synaptic signals (to speak very broadly) and then walks over to some DNA and does anything systematic to the DNA, to record the results of those signals, is storing something on the DNA. There could have been no way to get from one to the other, but now it appears that there is. Would it mean that memories (including cultural adaptations) could be passed from mother to child? No, for two reasons: (1) the DNA isn't being changed. (2) even if the DNA was being changed, it isn't in the germ-line. This is a crucial point: has anyone definitely ruled out the possibility that state of the gene regulation apparatus could somehow affect the germ line? This I am not clear about. When the Mom and Pop DNA really start to get down and boogie together, do they throw away the scratchpad that contains all the extra information about the state of the junk DNA, the methylation endcaps, etc? Or is it still an open question whether some of that can carry over? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Terren Suydam wrote: Hi Richard, Thanks for the link, pretty intriguing. It's important to note that the mechanism proposed is just a switch that turns specific genes off... so properly understood, it's likely that the resolution required to model this mechanism would not necessarily require modeling the entire DNA strand. It seems more likely that these methylation caps are being applied to very specific genes that produce proteins heavily implicated in the dynamics of synapse creation/destruction (or some other process related to memory). So modeling the phenomenon could very possibly be done functionally. Memories could only be passed to the child if 1) those DNA changes were also made in the germ cells (i.e. egg/sperm) and 2) the DNA changes involved resulted in a brain organization in the child that mimicked the parent's brain. (1) is very unlikely but theoretically possible; (2) is impossible for two reasons. One is, the methylation patterns proposed involve a large number of neurons, converging on a pattern of methylation; in contrast, a germ cell would only capture the methylation of a single cell (which would then be cloned in the developing fetus). Second, the hypothesized methylation patterns represent a different medium of information storage in the mature brain than what is normally considered to be the role of DNA in the developing brain. It would truly be a huge leap to suggest that the information stored via this alteration of DNA would result in that information being preserved somehow in a developing brain. There are plenty of other epigenetic phenomena to get Lamarck fans excited, but this isn't one of them. I see what you are saying. I really want to distance myself from this a little bit (don't want to seem like I am really holding the banner for Lamarck's crowd), but I think the main conclusion that we can draw from this piece of research is, as I said a moment ago, that we now have reason to believe that there is *some* mechanism that connects memories to DNA modifications, whereas if anyone had suggested such a link a few years ago they would have been speculating on thin ice. I definitely agree that getting from there to a situation in which packages of information are being inserted into germ cell DNA is a long road, but this one new piece of research has - surprisingly - just cut the length of that road in half. All fun and interesting, but now back to the real AGI Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
I don' really see how a change in gene expression in the nucleus of a neuron caused by methylation could store long term memories, since most neural network models store all most all their information in the location and differentiation of they synapses. How is information in a neural net stored by making what would appear to be only neuron-wide behaviors? Such a global change might be valuable for signally that a record of recent events in the neuron at a give brief period of time, should be stored, but it would not appear to actually keep them stored over a long period of time. I think the article failed to mention an important part of the theory of what is going on. Ed Porter -Original Message- From: Terren Suydam [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 12:16 PM To: agi@v2.listbox.com Subject: RE: [agi] Lamarck Lives!(?) Ed, That's a good point about synapses, but perhaps the methylation just affects the neuron's output, e.g., the targeted genes express proteins that only find a functional role in the axon. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Richard, The role played by the epigenome in genetics actually does have a slightly Lamarckian tinge. Nova had a show saying that when identical twins are born their epigenomes are very similar, but that as they age their epigenomes start to differ more an more, and that certain behaviors like drinking or smoking can increase the rate at which such changes take place. What I didn't understand about the article you linked to is that it appears they are changing the epigenome to change the expression of DNA, but as far as I know DNA only appears in the nucleus (with the exception of mitochondirial DNA), and thus would appear to affect the cell as a whole, and thus not be good at differentially affecting the strengths of different synapses --- as would presumably be required for most neuronal memory --- unless the nuclear DNA had some sort of mapping to individual synapses, or unless local changes to mitochondrial DNA, near a synapse are involved. The article does not appear to shed in any light on this issue of how changes in the expression of DNA would affect learning at the synapse level, where most people think it occurs. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 11:12 AM To: agi@v2.listbox.com Subject: [agi] Lamarck Lives!(?) Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on -your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
I definitely agree that getting from there to a situation in which packages of information are being inserted into germ cell DNA is a long road, but this one new piece of research has - surprisingly - just cut the length of that road in half. Half of infinity is still infinity ;-] It's just not a possibility, which should be obvious if you look at the quantity of information involved. Let M be a measure of the information stored via distributed methylation patterns across some number of neurons N. The amount of information stored by a single neuron's methylated DNA is going to be much smaller than M (roughly M/N). A single germ cell which might conceivably inherit the methylation pattern from some single neuron would not be able to convey any more than a [1/N] piece of the total information that makes up M. The real significance of this research has nothing to do with Lamarckian inheritance. It has to do with the proposed medium of memory, as a network of switched genes in neurons and perhaps other cells. It's a novel idea that is generative of a whole range of new hypotheses and applications (e.g. in the pharmaceutical space). Terren --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Terren Suydam wrote: I definitely agree that getting from there to a situation in which packages of information are being inserted into germ cell DNA is a long road, but this one new piece of research has - surprisingly - just cut the length of that road in half. Half of infinity is still infinity ;-] It's just not a possibility, which should be obvious if you look at the quantity of information involved. Let M be a measure of the information stored via distributed methylation patterns across some number of neurons N. The amount of information stored by a single neuron's methylated DNA is going to be much smaller than M (roughly M/N). A single germ cell which might conceivably inherit the methylation pattern from some single neuron would not be able to convey any more than a [1/N] piece of the total information that makes up M. Now you're just trying to make me think ;-). Okay, try this. [heck, you don't have to: I am just playing with ideas here...] The methylation pattern has not necessarily been shown to *only* store information in a distributed pattern of activation - the jury's out on that one (correct me if I'm wrong). Suppose that the methylation end caps are just being used as a way station for some mechanism whose *real* goal is to make modifications to some patterns in the junk DNA. So, here I am suggesting that the junk DNA of any particular neuron is being used to code for large numbers of episodic memories (one memory per DNA strand, say), with each neuron being used as a redundant store of many episodes. The same episode is stored in multiple neurons, but each copy is complete. When we observe changes in the methylation patterns, perhaps these are just part of the transit mechanism, not the final destination for the pattern. To put it in the language that Greg Bear would use, the endcaps were just part of the radio system. (http://www.gregbear.com/books/darwinsradio.cfm) Now suppose that part of the junk sequences that code for these memories are actually using a distributed coding scheme *within* the strand (in the manner of a good old fashioned backprop neural net, shall we say). That would mean that, contrary to what I said in the above paragraph, the individual strands were coding a bunch of different episodic memory traces, not just one. (It is even possible that the old idea of flashbulb memories may survive the critiques that have been launched against it ... and in that case, it could be that what we are talking about here is the mechanism for storing that particular set of memories. And in that case, perhaps the system expects so few of them, that all DNA strands everywhere in the system are dedicated to storing just the individual's store of flashbulb memories). Now, finally, suppose that there is some mechanism for radioing these memories to distribute them around the system ... and that the radio network extends as far as the germ DNA. Now, the offspring could get the mixed flashbulb memories of its parents, in perhaps very dilute or noisy form. This assumes that whatever coding scheme is used to store the information can somehow transcend the coding schemes used by different individuals. Since we do not yet know how much common ground there is between the knowledge storage used by individuals yet, this is still possible. There: I invented a possible mechanism. Does it work? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
Ed, Though it seems obvious that synapses are *involved* with memory storage, it's not proven that synapses individually *store* memories. Clearly memory is distributed, as evidenced by brain injury studies (a situation that led Karl Pribram/David Bohm to propose a holographic storage metaphor). In other words, memories might be stored as patterns of synaptic/neural dynamics, in which the relevant scope is well higher than at the level of the individual synapse. Given that memory storage is not so simple as to depend crucially on individual synapses, I see no serious problems with a neuron-wide mechanism of memory storage. Also, think of Hebbian learning, in which synaptic strength is reinforced based on a neuron-wide signal. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: From: Ed Porter [EMAIL PROTECTED] Subject: RE: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Wednesday, December 3, 2008, 1:33 PM I don' really see how a change in gene expression in the nucleus of a neuron caused by methylation could store long term memories, since most neural network models store all most all their information in the location and differentiation of they synapses. How is information in a neural net stored by making what would appear to be only neuron-wide behaviors? Such a global change might be valuable for signally that a record of recent events in the neuron at a give brief period of time, should be stored, but it would not appear to actually keep them stored over a long period of time. I think the article failed to mention an important part of the theory of what is going on. Ed Porter -Original Message- From: Terren Suydam [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 12:16 PM To: agi@v2.listbox.com Subject: RE: [agi] Lamarck Lives!(?) Ed, That's a good point about synapses, but perhaps the methylation just affects the neuron's output, e.g., the targeted genes express proteins that only find a functional role in the axon. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Richard, The role played by the epigenome in genetics actually does have a slightly Lamarckian tinge. Nova had a show saying that when identical twins are born their epigenomes are very similar, but that as they age their epigenomes start to differ more an more, and that certain behaviors like drinking or smoking can increase the rate at which such changes take place. What I didn't understand about the article you linked to is that it appears they are changing the epigenome to change the expression of DNA, but as far as I know DNA only appears in the nucleus (with the exception of mitochondirial DNA), and thus would appear to affect the cell as a whole, and thus not be good at differentially affecting the strengths of different synapses --- as would presumably be required for most neuronal memory --- unless the nuclear DNA had some sort of mapping to individual synapses, or unless local changes to mitochondrial DNA, near a synapse are involved. The article does not appear to shed in any light on this issue of how changes in the expression of DNA would affect learning at the synapse level, where most people think it occurs. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 11:12 AM To: agi@v2.listbox.com Subject: [agi] Lamarck Lives!(?) Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on -your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303
Re: [agi] Lamarck Lives!(?)
Ed, you seem to be taking the memory as synaptic weight modification model a bit too seriously ... it's really just a simplified formal model that captures a certain percentage of what goes on in the brain (and no one knows how much) This is why I shy away from brain-modeling approaches to AGI ... we just don't know how the brain works yet... ben g On Wed, Dec 3, 2008 at 1:33 PM, Ed Porter [EMAIL PROTECTED] wrote: I don' really see how a change in gene expression in the nucleus of a neuron caused by methylation could store long term memories, since most neural network models store all most all their information in the location and differentiation of they synapses. How is information in a neural net stored by making what would appear to be only neuron-wide behaviors? Such a global change might be valuable for signally that a record of recent events in the neuron at a give brief period of time, should be stored, but it would not appear to actually keep them stored over a long period of time. I think the article failed to mention an important part of the theory of what is going on. Ed Porter -Original Message- From: Terren Suydam [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 12:16 PM To: agi@v2.listbox.com Subject: RE: [agi] Lamarck Lives!(?) Ed, That's a good point about synapses, but perhaps the methylation just affects the neuron's output, e.g., the targeted genes express proteins that only find a functional role in the axon. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Richard, The role played by the epigenome in genetics actually does have a slightly Lamarckian tinge. Nova had a show saying that when identical twins are born their epigenomes are very similar, but that as they age their epigenomes start to differ more an more, and that certain behaviors like drinking or smoking can increase the rate at which such changes take place. What I didn't understand about the article you linked to is that it appears they are changing the epigenome to change the expression of DNA, but as far as I know DNA only appears in the nucleus (with the exception of mitochondirial DNA), and thus would appear to affect the cell as a whole, and thus not be good at differentially affecting the strengths of different synapses --- as would presumably be required for most neuronal memory --- unless the nuclear DNA had some sort of mapping to individual synapses, or unless local changes to mitochondrial DNA, near a synapse are involved. The article does not appear to shed in any light on this issue of how changes in the expression of DNA would affect learning at the synapse level, where most people think it occurs. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 11:12 AM To: agi@v2.listbox.com Subject: [agi] Lamarck Lives!(?) Am I right in thinking that what these people: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on -your-dna.html are saying is that memories can be stored as changes in the DNA inside neurons? If so, that would upset a few apple carts. Would it mean that memories (including cultural adaptations) could be passed from mother to child? Implication for neuroscientists proposing to build a WBE (whole brain emulation): the resolution you need may now have to include all the DNA in every neuron. Any bets on when they will have the resolution to do that? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com -- Ben Goertzel, PhD CEO, Novamente LLC and Biomind LLC Director of Research, SIAI [EMAIL PROTECTED] I intend to live forever, or die trying. -- Groucho Marx --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member
Re: [agi] Lamarck Lives!(?)
Does it work? Assuming that the encodings between parent and child are compatible, it could work. But you'd still be limited to the total amount of information storage allowable in the junk DNA (which would necessarily be a miniscule fraction of the total information stored in the brain as memory). And you'd still need to identify the mechanism that writes to the junk DNA, which would involve some hefty molecular machinery (snipping DNA, synthesizing the new stuff, rejoining it, all while doing error correction and turning off the error correction involved with normal DNA synthesis/repair). Finally, the idea of junk DNA is getting smaller and smaller as we identify gene targets that are not necessarily proteins, but various RNA products; or sections of DNA that are simply there to anchor other sections, or to enable other methods of gene switching. I know you're just playing here but it would be easy to empirically test this. Does junk DNA change between birth and death? Something tells me we would have discovered something that significant a long time ago. Terren --- On Wed, 12/3/08, Richard Loosemore [EMAIL PROTECTED] wrote: Okay, try this. [heck, you don't have to: I am just playing with ideas here...] The methylation pattern has not necessarily been shown to *only* store information in a distributed pattern of activation - the jury's out on that one (correct me if I'm wrong). Suppose that the methylation end caps are just being used as a way station for some mechanism whose *real* goal is to make modifications to some patterns in the junk DNA. So, here I am suggesting that the junk DNA of any particular neuron is being used to code for large numbers of episodic memories (one memory per DNA strand, say), with each neuron being used as a redundant store of many episodes. The same episode is stored in multiple neurons, but each copy is complete. When we observe changes in the methylation patterns, perhaps these are just part of the transit mechanism, not the final destination for the pattern. To put it in the language that Greg Bear would use, the endcaps were just part of the radio system. (http://www.gregbear.com/books/darwinsradio.cfm) Now suppose that part of the junk sequences that code for these memories are actually using a distributed coding scheme *within* the strand (in the manner of a good old fashioned backprop neural net, shall we say). That would mean that, contrary to what I said in the above paragraph, the individual strands were coding a bunch of different episodic memory traces, not just one. (It is even possible that the old idea of flashbulb memories may survive the critiques that have been launched against it ... and in that case, it could be that what we are talking about here is the mechanism for storing that particular set of memories. And in that case, perhaps the system expects so few of them, that all DNA strands everywhere in the system are dedicated to storing just the individual's store of flashbulb memories). Now, finally, suppose that there is some mechanism for radioing these memories to distribute them around the system ... and that the radio network extends as far as the germ DNA. Now, the offspring could get the mixed flashbulb memories of its parents, in perhaps very dilute or noisy form. This assumes that whatever coding scheme is used to store the information can somehow transcend the coding schemes used by different individuals. Since we do not yet know how much common ground there is between the knowledge storage used by individuals yet, this is still possible. There: I invented a possible mechanism. Does it work? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
I know you're just playing here but it would be easy to empirically test this. Does junk DNA change between birth and death? Something tells me we would have discovered something that significant a long time ago. Terren well, loads of mutations occur in nuclear DNA between birth and death; this is part of how aging occurs. There are specific DNA repair mechanisms that fix mutation errors that occur during the cell's lifetime It seems quite plausible that these repair mechanisms might work differently on coding and noncoding regions of the DNA ben g p.s. hmm.. relatedly, there is debatable evidence that in some cases there can be acquired mutations http://home.planet.nl/~gkorthof/kortho39.htm related to immune function, and some of these may be in genes and some not... --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Ben Goertzel wrote: I know you're just playing here but it would be easy to empirically test this. Does junk DNA change between birth and death? Something tells me we would have discovered something that significant a long time ago. Terren well, loads of mutations occur in nuclear DNA between birth and death; this is part of how aging occurs. There are specific DNA repair mechanisms that fix mutation errors that occur during the cell's lifetime It seems quite plausible that these repair mechanisms might work differently on coding and noncoding regions of the DNA Ah, hang on folks: what I was meaning was that the *state* of the junk DNA was being used, not the code. I am referring to the stuff that is dynamically interacting, as a result of which genes are switched on and off all over the place so this is a gigantic network of switches. I wouldn't suggest that something is snipping and recombining the actual code of the junk DNA, only that the state of the switches is being used to code for something. Question is: can the state of the switches be preserved during reproduction? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
On Wed, Dec 3, 2008 at 3:19 PM, Ed Porter [EMAIL PROTECTED] wrote: Terry and Ben, I never implied anything that could be considered a memory at a conscious level is stored at just one synapse, but all the discussions I have heard of learning in various brain science books and lectures imply synaptic weights are the main place of our memories are stored. Nevertheless, although it's an oft-repeated and well-spread meme, the available biological evidence shows only that **this is one aspect of the biological basis of memory in organisms with complex brains** There certainly is data about long-term potentiation and its relationship to memory ... but the available data comes nowhere near to justifying the sorts of assumptions made in setting up formal neural net models, in which synaptic modification is assumed as the sole basis of learning/memory... ben g --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
Terry and Ben, I never implied anything that could be considered a memory at a conscious level is stored at just one synapse, but all the discussions I have heard of learning in various brain science books and lectures imply synaptic weights are the main place of our memories are stored. Yes, Hebbian learning would appear to use a neuron wide signal that a neuron has fired, but the actual Hebbian learning is only believed to take place at individual synapses as a function of the relationship of the timing between the synapse's up- and downstream neurons. So all the Hebbian and Hebbian-like learning I have ever heard described distinguishes between which of a neuron's synapses are to have their weights changed by how much and/or in what direction. Now there may well be other mechanisms which would allow long term memory to be stored at a neuron-wide level, but I can't at the moment remember reading or hearing of any. That is not proof they don't exist, but it, at least it suggests that, so far, the evidence for such mechanism that has been learned is underwhelming. On the other hand, I have read or heard probably at least a thousand times about the brain storing information in synapses. Ed Porter -Original Message- From: Terren Suydam [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 2:00 PM To: agi@v2.listbox.com Subject: RE: [agi] Lamarck Lives!(?) Ed, Though it seems obvious that synapses are *involved* with memory storage, it's not proven that synapses individually *store* memories. Clearly memory is distributed, as evidenced by brain injury studies (a situation that led Karl Pribram/David Bohm to propose a holographic storage metaphor). In other words, memories might be stored as patterns of synaptic/neural dynamics, in which the relevant scope is well higher than at the level of the individual synapse. Given that memory storage is not so simple as to depend crucially on individual synapses, I see no serious problems with a neuron-wide mechanism of memory storage. Also, think of Hebbian learning, in which synaptic strength is reinforced based on a neuron-wide signal. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: From: Ed Porter [EMAIL PROTECTED] Subject: RE: [agi] Lamarck Lives!(?) To: agi@v2.listbox.com Date: Wednesday, December 3, 2008, 1:33 PM I don' really see how a change in gene expression in the nucleus of a neuron caused by methylation could store long term memories, since most neural network models store all most all their information in the location and differentiation of they synapses. How is information in a neural net stored by making what would appear to be only neuron-wide behaviors? Such a global change might be valuable for signally that a record of recent events in the neuron at a give brief period of time, should be stored, but it would not appear to actually keep them stored over a long period of time. I think the article failed to mention an important part of the theory of what is going on. Ed Porter -Original Message- From: Terren Suydam [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 12:16 PM To: agi@v2.listbox.com Subject: RE: [agi] Lamarck Lives!(?) Ed, That's a good point about synapses, but perhaps the methylation just affects the neuron's output, e.g., the targeted genes express proteins that only find a functional role in the axon. Terren --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Richard, The role played by the epigenome in genetics actually does have a slightly Lamarckian tinge. Nova had a show saying that when identical twins are born their epigenomes are very similar, but that as they age their epigenomes start to differ more an more, and that certain behaviors like drinking or smoking can increase the rate at which such changes take place. What I didn't understand about the article you linked to is that it appears they are changing the epigenome to change the expression of DNA, but as far as I know DNA only appears in the nucleus (with the exception of mitochondirial DNA), and thus would appear to affect the cell as a whole, and thus not be good at differentially affecting the strengths of different synapses --- as would presumably be required for most neuronal memory --- unless the nuclear DNA had some sort of mapping to individual synapses, or unless local changes to mitochondrial DNA, near a synapse are involved. The article does not appear to shed in any light on this issue of how changes in the expression of DNA would affect learning at the synapse level, where most people think it occurs. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent
RE: [agi] Lamarck Lives!(?)
Richard, You asked can the state of the switches be preserved during reproduction? According to the Nova show I saw about epigenome, they were able to induce a change in a mouse's epigenome that changed its appearance, then its children would be more likely to inherit the same changed appearance. They could also unchanged that particular epigenomic trait back to what it had been in a parent or grandparent. So they were able to change and unchanged traits that were inheritable. So the answer is yes. Ed Porter -Original Message- From: Richard Loosemore [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 2:44 PM To: agi@v2.listbox.com Subject: Re: [agi] Lamarck Lives!(?) Ben Goertzel wrote: I know you're just playing here but it would be easy to empirically test this. Does junk DNA change between birth and death? Something tells me we would have discovered something that significant a long time ago. Terren well, loads of mutations occur in nuclear DNA between birth and death; this is part of how aging occurs. There are specific DNA repair mechanisms that fix mutation errors that occur during the cell's lifetime It seems quite plausible that these repair mechanisms might work differently on coding and noncoding regions of the DNA Ah, hang on folks: what I was meaning was that the *state* of the junk DNA was being used, not the code. I am referring to the stuff that is dynamically interacting, as a result of which genes are switched on and off all over the place so this is a gigantic network of switches. I wouldn't suggest that something is snipping and recombining the actual code of the junk DNA, only that the state of the switches is being used to code for something. Question is: can the state of the switches be preserved during reproduction? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Possibly... it has been shown with methylation. But I think the mechanism you're proposing could not involve methylation because (someone can correct me if wrong) methylation is only applicable to coding regions (methyl group only added to specific DNA sequences that mark the gene). That's not to say another switching mechanism on non-coding regions could not also be heritable (i.e., reproduced in the copied DNA strand). Using DNA switches (such as methylation) is more tractable than DNA rewriting, but again, the amount of information storage is the limiting factor. Indeed, switching on and off sections of DNA implies a big reduction in information capacity (as compared to DNA rewriting), since gene switching applies to sections of DNA. I wonder how much memory would you expect to be able to pass on through this mechanism? Also, you would need to propose the mechanism by which this form of storage would be read. Since junk DNA by definition doesn't code for anything, by what mechanism would these switches have an effect on cellular, neural, or otherwise cognitive processes? Terren --- On Wed, 12/3/08, Richard Loosemore [EMAIL PROTECTED] wrote: Ah, hang on folks: what I was meaning was that the *state* of the junk DNA was being used, not the code. I am referring to the stuff that is dynamically interacting, as a result of which genes are switched on and off all over the place so this is a gigantic network of switches. I wouldn't suggest that something is snipping and recombining the actual code of the junk DNA, only that the state of the switches is being used to code for something. Question is: can the state of the switches be preserved during reproduction? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Junk DNA doesn't code for protein, but it seems to carry out various control functions over the protein synthesis and interaction processes, no? ben g On Wed, Dec 3, 2008 at 4:02 PM, Terren Suydam [EMAIL PROTECTED] wrote: Possibly... it has been shown with methylation. But I think the mechanism you're proposing could not involve methylation because (someone can correct me if wrong) methylation is only applicable to coding regions (methyl group only added to specific DNA sequences that mark the gene). That's not to say another switching mechanism on non-coding regions could not also be heritable (i.e., reproduced in the copied DNA strand). Using DNA switches (such as methylation) is more tractable than DNA rewriting, but again, the amount of information storage is the limiting factor. Indeed, switching on and off sections of DNA implies a big reduction in information capacity (as compared to DNA rewriting), since gene switching applies to sections of DNA. I wonder how much memory would you expect to be able to pass on through this mechanism? Also, you would need to propose the mechanism by which this form of storage would be read. Since junk DNA by definition doesn't code for anything, by what mechanism would these switches have an effect on cellular, neural, or otherwise cognitive processes? Terren --- On Wed, 12/3/08, Richard Loosemore [EMAIL PROTECTED] wrote: Ah, hang on folks: what I was meaning was that the *state* of the junk DNA was being used, not the code. I am referring to the stuff that is dynamically interacting, as a result of which genes are switched on and off all over the place so this is a gigantic network of switches. I wouldn't suggest that something is snipping and recombining the actual code of the junk DNA, only that the state of the switches is being used to code for something. Question is: can the state of the switches be preserved during reproduction? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com -- Ben Goertzel, PhD CEO, Novamente LLC and Biomind LLC Director of Research, SIAI [EMAIL PROTECTED] I intend to live forever, or die trying. -- Groucho Marx --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
Ben, I basically agree. There many things going in the human brain. There are all the different neuro- chemicals, receptors, and blockers, some of which are not only effective across individual synapses, but often across broader distances. There is the fact that neuron branches can apparently grow in directions guided by chemical gradients. There are synchronies and brain waves, and the way in which they might spatially encode or decode information. And so on. So I admit the brain is much more complicated than most neural net models. But I have not seen any explanation of how changes in gene expression in a neuron's nucleus would store memories, even given the knowledge that the epigenome can store information. If there is such an explanation, either now or in the future, I would welcome hearing it. Ed Porter -Original Message- From: Ben Goertzel [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 3:24 PM To: agi@v2.listbox.com Subject: Re: [agi] Lamarck Lives!(?) On Wed, Dec 3, 2008 at 3:19 PM, Ed Porter [EMAIL PROTECTED] wrote: Terry and Ben, I never implied anything that could be considered a memory at a conscious level is stored at just one synapse, but all the discussions I have heard of learning in various brain science books and lectures imply synaptic weights are the main place of our memories are stored. Nevertheless, although it's an oft-repeated and well-spread meme, the available biological evidence shows only that **this is one aspect of the biological basis of memory in organisms with complex brains** There certainly is data about long-term potentiation and its relationship to memory ... but the available data comes nowhere near to justifying the sorts of assumptions made in setting up formal neural net models, in which synaptic modification is assumed as the sole basis of learning/memory... ben g --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
http://en.wikipedia.org/wiki/Epigenetic_inheritance#DNA_methylation_and_chromatin_remodeling The DNA sites where methylation can occur are rare, except in the regions where gene transcription occurs... which generally supports what I was saying about coding regions. However it is certainly possible that a different (as yet undiscovered) enzyme could methylate a different section of DNA that has no correlation at all with transcription. The key point is that it's certainly possible in principle to have some kind of signaling mechanism that uses junk DNA as a substrate, and which can be inherited epigenetically. It doesn't seem likely that methylation (as we know it) fits the bill, so probably Richard would require an as yet unknown mechanism for switching junk DNA. --- On Wed, 12/3/08, Ben Goertzel [EMAIL PROTECTED] wrote: Junk DNA doesn't code for protein, but it seems to carry out various control functions over the protein synthesis and interaction processes, no? ben g On Wed, Dec 3, 2008 at 4:02 PM, Terren Suydam [EMAIL PROTECTED] wrote: Possibly... it has been shown with methylation. But I think the mechanism you're proposing could not involve methylation because (someone can correct me if wrong) methylation is only applicable to coding regions (methyl group only added to specific DNA sequences that mark the gene). That's not to say another switching mechanism on non-coding regions could not also be heritable (i.e., reproduced in the copied DNA strand). Using DNA switches (such as methylation) is more tractable than DNA rewriting, but again, the amount of information storage is the limiting factor. Indeed, switching on and off sections of DNA implies a big reduction in information capacity (as compared to DNA rewriting), since gene switching applies to sections of DNA. I wonder how much memory would you expect to be able to pass on through this mechanism? Also, you would need to propose the mechanism by which this form of storage would be read. Since junk DNA by definition doesn't code for anything, by what mechanism would these switches have an effect on cellular, neural, or otherwise cognitive processes? Terren --- On Wed, 12/3/08, Richard Loosemore [EMAIL PROTECTED] wrote: Ah, hang on folks: what I was meaning was that the *state* of the junk DNA was being used, not the code. I am referring to the stuff that is dynamically interacting, as a result of which genes are switched on and off all over the place so this is a gigantic network of switches. I wouldn't suggest that something is snipping and recombining the actual code of the junk DNA, only that the state of the switches is being used to code for something. Question is: can the state of the switches be preserved during reproduction? Richard Loosemore --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com -- Ben Goertzel, PhD CEO, Novamente LLC and Biomind LLC Director of Research, SIAI [EMAIL PROTECTED] I intend to live forever, or die trying. -- Groucho Marx --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
RE: [agi] Lamarck Lives!(?)
I think the key is to see the gene switching not as an information store per se but as part of a larger dynamic process (which might be similar in principle to simulated annealing), in which the contributions of whole neurons (e.g., the outputs) are switched in some way meaningful to the dynamic. --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Ben, I basically agree. There many things going in the human brain. There are all the different neuro- chemicals, receptors, and blockers, some of which are not only effective across individual synapses, but often across broader distances. There is the fact that neuron branches can apparently grow in directions guided by chemical gradients. There are synchronies and brain waves, and the way in which they might spatially encode or decode information. And so on. So I admit the brain is much more complicated than most neural net models. But I have not seen any explanation of how changes in gene expression in a neuron's nucleus would store memories, even given the knowledge that the epigenome can store information. If there is such an explanation, either now or in the future, I would welcome hearing it. Ed Porter -Original Message- From: Ben Goertzel [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 3:24 PM To: agi@v2.listbox.com Subject: Re: [agi] Lamarck Lives!(?) On Wed, Dec 3, 2008 at 3:19 PM, Ed Porter [EMAIL PROTECTED] wrote: Terry and Ben, I never implied anything that could be considered a memory at a conscious level is stored at just one synapse, but all the discussions I have heard of learning in various brain science books and lectures imply synaptic weights are the main place of our memories are stored. Nevertheless, although it's an oft-repeated and well-spread meme, the available biological evidence shows only that **this is one aspect of the biological basis of memory in organisms with complex brains** There certainly is data about long-term potentiation and its relationship to memory ... but the available data comes nowhere near to justifying the sorts of assumptions made in setting up formal neural net models, in which synaptic modification is assumed as the sole basis of learning/memory... ben g --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com agi | Archives | Modify Your Subscription --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Yes. Ed etc., what comes to mind is Eugene Ishikevich (sp?) 's nonlinear dynamics models of fast and slow dynamics in neurons, which are based on ion channel models similar to (but more sophisticated in some cases than) the classic Hodgkin-Huxley equations Potentially the gene switching under discussion could affect some of the parameters in Ishikevich's equations, thus modifying the behavior of neurons. In Ishikevich's equations, classic LTP would take the form of modifying certain of the equational parameters, whereas this gene switching could take the form of modifying others. Note, I'm not selling Ishikevich's stuff as a final and correct model of neurodynamics -- just pointing it out as one interesting brain model that potentially would explain how these gene switches could conceivable affect learning via affecting holistic brain dynamics ... attractors and all that fun stuff... -- Ben G On Wed, Dec 3, 2008 at 5:12 PM, Terren Suydam [EMAIL PROTECTED] wrote: I think the key is to see the gene switching not as an information store per se but as part of a larger dynamic process (which might be similar in principle to simulated annealing), in which the contributions of whole neurons (e.g., the outputs) are switched in some way meaningful to the dynamic. --- On Wed, 12/3/08, Ed Porter [EMAIL PROTECTED] wrote: Ben, I basically agree. There many things going in the human brain. There are all the different neuro- chemicals, receptors, and blockers, some of which are not only effective across individual synapses, but often across broader distances. There is the fact that neuron branches can apparently grow in directions guided by chemical gradients. There are synchronies and brain waves, and the way in which they might spatially encode or decode information. And so on. So I admit the brain is much more complicated than most neural net models. But I have not seen any explanation of how changes in gene expression in a neuron's nucleus would store memories, even given the knowledge that the epigenome can store information. If there is such an explanation, either now or in the future, I would welcome hearing it. Ed Porter -Original Message- From: Ben Goertzel [mailto:[EMAIL PROTECTED] Sent: Wednesday, December 03, 2008 3:24 PM To: agi@v2.listbox.com Subject: Re: [agi] Lamarck Lives!(?) On Wed, Dec 3, 2008 at 3:19 PM, Ed Porter [EMAIL PROTECTED] wrote: Terry and Ben, I never implied anything that could be considered a memory at a conscious level is stored at just one synapse, but all the discussions I have heard of learning in various brain science books and lectures imply synaptic weights are the main place of our memories are stored. Nevertheless, although it's an oft-repeated and well-spread meme, the available biological evidence shows only that **this is one aspect of the biological basis of memory in organisms with complex brains** There certainly is data about long-term potentiation and its relationship to memory ... but the available data comes nowhere near to justifying the sorts of assumptions made in setting up formal neural net models, in which synaptic modification is assumed as the sole basis of learning/memory... ben g --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com agi | Archives | Modify Your Subscription agi | Archives | Modify Your Subscription -- Ben Goertzel, PhD CEO, Novamente LLC and Biomind LLC Director of Research, SIAI [EMAIL PROTECTED] I intend to live forever, or die trying. -- Groucho Marx --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html Actually, this makes sense. It explains most of the discrepancy between the 10^9 bits of human long term memory estimated by Landauer and the 10^15 synapses in the human brain. If memory is stored in neurons (by gene regulation to control activation threshold), then you have only 10^11 bits of storage, or 1 bit per neuron. Here is how it could work. Imagine a neural network with fixed, randomly weighted synapses. Then insert a neuron at each synapse with one input and one output. Then you could apply Hebbian learning by modifying the conductivity of the middle neuron. If the input and output neurons fire at the same time, then the middle neuron would lower its threshold if both weights are the same, or raise it if the weights have opposite sign. In other words, instead of A - B with a variable weight, you have A - M - B with a middle neuron M of variable conductivity and two fixed weights. Of course real neurons have thousands of inputs and outputs. This means that there are thousands of neurons between A and B, and these middle neurons connect to thousands of others. If these connections are random, then Hebbian learning applied to these thousands of middle neurons would correlate only with AB and create minor noise for other neurons. -- Matt Mahoney, [EMAIL PROTECTED] --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
Re: [agi] Lamarck Lives!(?)
Well, LTP is definitely real ... and I'm quite sure the scheme you describe is *not* how learning works in the brain ;-) ,,, but I'm equally sure that the full story has not yet been uncovered... ben On Wed, Dec 3, 2008 at 5:25 PM, Matt Mahoney [EMAIL PROTECTED] wrote: http://www.newscientist.com/article/mg20026845.000-memories-may-be-stored-on-your-dna.html Actually, this makes sense. It explains most of the discrepancy between the 10^9 bits of human long term memory estimated by Landauer and the 10^15 synapses in the human brain. If memory is stored in neurons (by gene regulation to control activation threshold), then you have only 10^11 bits of storage, or 1 bit per neuron. Here is how it could work. Imagine a neural network with fixed, randomly weighted synapses. Then insert a neuron at each synapse with one input and one output. Then you could apply Hebbian learning by modifying the conductivity of the middle neuron. If the input and output neurons fire at the same time, then the middle neuron would lower its threshold if both weights are the same, or raise it if the weights have opposite sign. In other words, instead of A - B with a variable weight, you have A - M - B with a middle neuron M of variable conductivity and two fixed weights. Of course real neurons have thousands of inputs and outputs. This means that there are thousands of neurons between A and B, and these middle neurons connect to thousands of others. If these connections are random, then Hebbian learning applied to these thousands of middle neurons would correlate only with AB and create minor noise for other neurons. -- Matt Mahoney, [EMAIL PROTECTED] --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?; Powered by Listbox: http://www.listbox.com -- Ben Goertzel, PhD CEO, Novamente LLC and Biomind LLC Director of Research, SIAI [EMAIL PROTECTED] I intend to live forever, or die trying. -- Groucho Marx --- agi Archives: https://www.listbox.com/member/archive/303/=now RSS Feed: https://www.listbox.com/member/archive/rss/303/ Modify Your Subscription: https://www.listbox.com/member/?member_id=8660244id_secret=120640061-aded06 Powered by Listbox: http://www.listbox.com
