Comments on: Neuroengineering memory: Something old, something new http://neurodudes.com/2009/04/13/neuroengineering-memory-something-old-something-new/ at the intersection of neuroscience and AI. Tue, 07 Sep 2010 05:45:01 +0000 http://wordpress.org/?v=2.9.2 hourly 1 By: Todd Sacktor http://neurodudes.com/2009/04/13/neuroengineering-memory-something-old-something-new/comment-page-1/#comment-821159 Todd Sacktor Mon, 20 Apr 2009 03:52:32 +0000 http://neurodudes.com/?p=619#comment-821159 Neville, PKMzeta actually works specifically on GluR2-dependent trafficking, as shown in Yao et al., PKM? maintains late-LTP by NSF/GluR2-dependent trafficking of postsynaptic AMPARs, J. Neurosci., 28:7820-7827 (2008). And yes, its effect is specific to the synapses undergoing LTP. Neville, PKMzeta actually works specifically on GluR2-dependent trafficking, as shown in Yao et al., PKM? maintains late-LTP by NSF/GluR2-dependent trafficking of postsynaptic AMPARs, J. Neurosci., 28:7820-7827 (2008). And yes, its effect is specific to the synapses undergoing LTP.

]]> By: Neville http://neurodudes.com/2009/04/13/neuroengineering-memory-something-old-something-new/comment-page-1/#comment-821156 Neville Mon, 20 Apr 2009 03:04:23 +0000 http://neurodudes.com/?p=619#comment-821156 Todd, thanks for taking the time to read and respond to the post. And for the answer to my question about mechanisms! So, PKMzeta adds more AMPA receptors to maintain the memory? I assume this is synapse-specific, correct? (ie. not doubling AMPA at all synaptic sites but rather at specific sites) If you have any pointers to this literature about how PKMzeta works (at least to the degree it is currently known) and its effects on memory-specific synapses and spines, I'd love to read more on this. I myself am working on a project right now involving RNA editing of GluR2, so I'd like to learn more. You make a good point about the CREB study. Still, as a genetic tool, CREB overexpression is, currently, unique in allow us to control which neurons are part of a memory. For that alone, the study is fascinating, but it is hard not to speculate about pathways and mechanisms involved in memory storage. Thanks for the inspiring work and for contributing to the discussion here at Neurodudes! And folks, given what Todd mentioned about PKMzeta increasing the size of spines, I think this is the first time we've had "fresh science" featured on ND. And a hot topic at that! :) Todd, thanks for taking the time to read and respond to the post. And for the answer to my question about mechanisms! So, PKMzeta adds more AMPA receptors to maintain the memory? I assume this is synapse-specific, correct? (ie. not doubling AMPA at all synaptic sites but rather at specific sites) If you have any pointers to this literature about how PKMzeta works (at least to the degree it is currently known) and its effects on memory-specific synapses and spines, I’d love to read more on this. I myself am working on a project right now involving RNA editing of GluR2, so I’d like to learn more.

You make a good point about the CREB study. Still, as a genetic tool, CREB overexpression is, currently, unique in allow us to control which neurons are part of a memory. For that alone, the study is fascinating, but it is hard not to speculate about pathways and mechanisms involved in memory storage. Thanks for the inspiring work and for contributing to the discussion here at Neurodudes!

And folks, given what Todd mentioned about PKMzeta increasing the size of spines, I think this is the first time we’ve had “fresh science” featured on ND. And a hot topic at that! :)

]]> By: Todd Sacktor http://neurodudes.com/2009/04/13/neuroengineering-memory-something-old-something-new/comment-page-1/#comment-821010 Todd Sacktor Sat, 18 Apr 2009 20:24:32 +0000 http://neurodudes.com/?p=619#comment-821010 Neville, Just to let you know, the work that The Times mostly referred to was our 2006, not our 2007 Science article. PKMzeta works on glutamate receptor (AMPA receptor, GluR2 subunit) trafficking, a component of which cycles within minutes into and out of the synapse. PKMzeta acts to continually shift the distribution, doubling the number of postsynaptic receptors. The continual activity of the enzyme is required for maintaining the doubling and thus the memory. PKMzeta also maintains an increase in the size of spines, but this is not yet published. The CREB study shows that destruction of the specific neurons that were active during memory formation wipes out the memory retention. It does not address the mechanism of memory storage per se. Neville, Just to let you know, the work that The Times mostly referred to was our 2006, not our 2007 Science article. PKMzeta works on glutamate receptor (AMPA receptor, GluR2 subunit) trafficking, a component of which cycles within minutes into and out of the synapse. PKMzeta acts to continually shift the distribution, doubling the number of postsynaptic receptors. The continual activity of the enzyme is required for maintaining the doubling and thus the memory. PKMzeta also maintains an increase in the size of spines, but this is not yet published.

The CREB study shows that destruction of the specific neurons that were active during memory formation wipes out the memory retention. It does not address the mechanism of memory storage per se.

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