Sturla Molden wrote:
> There is no evidence that LTP is a naturally occuring
Would you care to square this with what I posted in respons to Walter, above.
The research report I read did clearly state that Ca(2+) dynamics above a
threshold have "staying power" (my words)... that is, their effects continue
after the sub-threshold ionic flow has ceased. What, if anything but an
LTP-like effect, is this?
> It araises from repeated tetanisation of
> specific neural pathways, eg. in the hippocampus. It is
> also not a homogenous phenomenon, there are several
> sub-types of LTP depending on different receptors
> (eg the NMDA receptor, opioid receptors, mGluRs)
> and with different durations.
>> LTP depend on the same mechanisms that seem to be
> involved in memory formation, but there is no evidence
> that LTP is the substrate for memory.
Yeah, but show me "memory" without the involvement of LTP... only way one can
is to show me a "corpse" (brain dead).
> Theoretical models of associative memory are very
> robust with respect to the choise of plasticity
> mechanism, and a number of different mechanisms
> will do the job equally well. Neurons do also
> express different types of plasticities, not just
> linear scaling of synaptic weights.
Of course, it's kind of hard to "draw a picture" using only "straight lines".
> There is no reason to believe that Altzheimer patients
> have impaired memory because they lack LTP. If they
> do lack LTP, one should rather say that they are
> impaired on synaptic plasticity.
This can't be said... all that can be said is the hypothesis must be tested
if anything's to be said.
> The hypothesis LTP = memory is far from proven.
Has anyone in this thread said such?
> It is supported by virtually no experimental
> evidence. I do think it is more likely that LTP
> is an emergent phenomenon araising from massive
> recruitment of neural plasticity apparatuses
> due to the teanising stimuli; the real mechanisms
> of memory - which is the natural output from
> the cellular pasticity apparatuses - are small
> and inconspicous.
But they're all that's necessary... and how could they possibly be isolated
from LTP, therefore "making" LTP to be as you say?
> And as long as single-unit studies show several
> mechanisms of plsticity in single cortical neurons
> and the theoreticl models work equally well with
> a number o diffferent forms of plsticity, there
> is no reason to suspect that Altzheimer's
> patients are impaired on memory because they are
> impaired on LTP.
It must be tested before such can be said.
> It is just as possible that
> they are impaired on LTP because they are
> impaired on memory (neuronal plsticity).
I don't disagree with you on this last point, but it, too, must be tested.