[Neuroscience] Re: Long-term potentiation and depression
(by r_s_norman from _comcast.net)
Sun Jun 15 09:00:34 EST 2008
On Sat, 14 Jun 2008 18:30:37 -0700 (PDT), Bill
<connelly.bill from gmail.com> wrote:
>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.
>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.
OK, to be more specific: I would look more at the way that last, key
step works than at the route taken. So if several routes all
ultimately increase the number of post-synaptic receptors at a site
then they are the "same" mechanism at least in so far as the result of
increasing synaptic efficacy. However, changing the specific
molecular form of a receptor while also building in number is a
different mechanism, as is adding any other synaptic structure or
building the size of the synapse even though the number of receptors
is still increased.
I still think that what we ordinarily call permanent "learning" or
"memory" differs in mechanism in this sense than the factors that
cause the long term potentiation that lasts hours and days.
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