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=8660244&id_secret=123753653-47f84b Powered by Listbox: http://www.listbox.com
