[Neuroscience] Re: Long-term potentiation and depression

Bill via neur-sci%40net.bio.net (by connelly.bill from gmail.com)
Sat Jun 14 18:13:37 EST 2008


On Jun 15, 12:35 am, usene... from out-of-phase.de (Christian Wilms) wrote:
> Bill <connelly.b... from gmail.com> wrote:
> > People often put bicucculine in the mix because if you're having
> > trouble getting LTP (ot at least maintaining it), you put a GABA(A)
> > blocker in the mix and you often get it.
>
> Wouldn't that imply that one is stimulating inhibitory input as well and
> thus possibly not only inducing plasticity in the excitatory path, but
> also in the inhibitory path. That would do quite a good job at
> complicating the results.
>
> Best, Chris

Well I don't think there is any doubt that field stimulation in the
hippocampus recruits (often powerful) inhibition, whether directly or
or via the local circuit. I get your meaning, but I definately know of
LTP researchers who think adding a GABA(A) antagonist is cheating.
When you're looking at field EPSPs GABAergic inhibtion has almost no
impact on the size or kinetics of the event, so you are essentially
looking at a selective glutamatergic event. (While of course I
appreciate GABA will be having large impacts of the integration of
said EPSP).

With field stimulation, in the presence of of GABA blockade, you often
get epileptiform activity, so you're confounding things that way as
well.

If you were looking at spike timing dependent plasticity, and were
only recruiting a single axon, then you'd be fine in blocking GABA, as
your source of (back propagating) AP formation is your current
injection. But if you're hoping to recruit the APs with field
stimulation, then GABA(A) blockade is going to be doing some odd stuff.


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