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Sun Apr 10 21:39:47 EST 2005

carrying through a more-detailed version of the things I've discussed above (it's
how I think about everything within the nervous system) there must be a
correlation. If the activation that normally empowers Ca(2+) dynamics is thrown
out of balance, then the Ca(2+) dynamics must also be thrown out of balance. What
I cannot say is whether it is a causative correlation... I cannot say that
LTP-dis-integration (or any other broken "normal" neural functionality) causes
Alzheimer's... (could be a disease agent that results in both) I expect that it
can, but I cannot say that it would be the only way that the normal functioning
of the neural substrate of Alzheimer's can be caused to go willy-nilly. (The
article I read did address things genetic, and, if I recall correctly, seemed to
rule that out a genetic basis for the Ca(2+) observables.)

> What implications this has are sketchy at best. It is an
> interesting possibility though, that memory related dysfunction in AD
> patients MIGHT be related to LTP deficits. But I admit this assumes both that
> LTP=memory and that AD has an effect on LTP in human patients.
> >
> > > The hypothesis LTP = memory is far from proven.
> >
> > Has anyone in this thread said such?
> >
> I'm looking for references (hint,hint:-)). It would be a good
> side issue to discuss, the critique of the notion that LTP and
> memory have a significant overlap.

Neural activation, of which LTP is but a tiny component, and memory =must= have
100% overlap... else one's left having to once again, postulate a "black box"
where "magic" happens. (In my work, BTW, I've implicated neuralglia in memory
because of the role they play in ionic conductances, and their contractile
properties, which alter the 3-D geometry of the flow inherent in ionic

> > > 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.
> >

You need to get together with whoever posted the above.

> Here is where I would ask whether convergence of presynaptic input onto a
> postsynaptic neuron is analogous to the tetanization or theta bursts used in
> experimental LTP induction. If this putative convergence can bring about
> similar results (e.g.- depolarization to a potential that alleviates the
> magnesium block on the NMDA receptor) then we have a good point for further
> discussion. In this case an LTP or LTP-like phenomenon might be involved in
> natural synaptic activity of hippocampal areas implicated in memory
> processing. Of course this assumes LTP = memory and that memory and a certain
> region of hippocampus are related.

It can be said with absolute-certainty that LTP does not equal "memory" because
neither LTP, nor any other discretely-identifiable neural activation could, in
and of itself, possibly yield minimal 3-D-preserving, asymmetry-compensating

> > But they're all that's necessary... and how could they
> possibly be isolated
> > from LTP, therefore "making" LTP to be as you say?
> >
> Can said synaptic plasticity be broken into relatively discrete components
> (e.g. facilitation versus potentiation).

??? :-)

> Remember the temporaldistinctions
> also. Plus would these "discrete components" be relatively independent of
> eachother? Or would one set the stage for the next?

Nothing within a fully-functional nervous system constitutes a "discrete
component". Folks can artificially isolate upon this or that, but then they've
got to find out how, where and why, what they've observed fits into the geometry
that I've discussed above. Nervous systems are
fantastically-tightly-integrated... isolating on this or that is, of course,
useful, especially with respect to converging upon explanations of organic
dysfunction, but fully-functional nervous systems require that everything be
fully-cross-correlated... integrated.

Again, the following is from someone else.

> > > 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.
> I still would like some good references that critique the LTP = memory
> notion.

Other than what I've shared with you, here, you won't get such from me.

> I've been too busy over this last week to study LTP, but this weekend
> I'll dive deeper into the literature and complex issues.
> > It must be tested before such can be said.
> >
> Agreed. I've had trouble finding anything that discusses LTP
> and AD in the same breath, besides a couple transgenic model
> studies.
> >
> > > 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.
> >
> >
> >
> I'll get back into this thread over the weekend. Everybody's
> input has been very helpful.
> --
> Scott Chase (note followups at anthym at webtv.net)

Final comment: I can expand the brief discussion I've posted here on and on.
Since it's stuff came together, I've not come across any experimental paper to
which it cannot be applied robustly, always yielding new insights and stimulating
desired modifications to the experimental design that would, themselves, yield
more of the same, ad infinitum (on the technicality that the 3 factors are
infinitely-divisible, of course one stops before over-cooking any particular
insight, but the insights branch, and become ever-more-prolific in the same way).
I think every grad student in Neuroscience should have what's here... 'course I'm
"prejudiced :-). Thanks for the opportunity to discuss. Cheers, Scott, ken

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