[Neuroscience] Re: Long-term potentiation and depression

Bill via neur-sci%40net.bio.net (by connelly.bill from gmail.com)
Sat Jun 14 20:30:37 EST 2008

Hm, I suppose you're right. Initially I wrote this post disagreeing
with you, but as I explored the following analogy, I changed my mind
to a degree. Would you say, that the people in Hiroshima who were
vaporised directly by the high density of photons, and those that died
six weeks later from radiation poisoning were killed by the same
mechanism. You could argue that they were (the mechanism being a
nuclear explosion) or you could argue that they weren't.

I thought you were meaning that while an NMDA-R dependent mechanism
causes an initial change in synaptic weights in the hippocampus/MTL
sturctures, but the distribution of the engram throughout the cortex
require something completely different.

On Jun 15, 11:20 am, r norman <r_s_norman from _comcast.net> wrote:
> Once you start a second messenger cell signaling pathway, what you
> call a "different" mechanism becomes much a matter of philosophy.  If
> you temporarily upregulate a synaptic receptor pathway so that the
> effect lasts hours or days until protein turnover restores it to the
> old value, is that a different mechanism from one that activates a
> different kind of gene switch that can last forever but still uses a
> number of the same intermediaries?  I would call these different.

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