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
