IUBio

pathology of epilepsy

Matt Jones jonesmat at ohsu.edu
Mon Sep 21 11:57:51 EST 1998


In article <6u0i74$6ev at dfw-ixnews6.ix.netcom.com> F. Frank LeFever,
flefever at ix.netcom.com writes:
>I appreciate Matt's elaboration, and his referencer to Kapur &
>MacDonald, which I intend to look into: my own special interest is in
>long-term consequences of MILD head injury, which raises seizure risk
>only very slightly, compared to severe injury.  Interestingly, data
>

Frank, I hope you can read this message amidst the nonscience and
spam-bot posts.

If you are interested in the effects of mild head injury, you may also
want to check out recent papers by Ivan Soltesz and colleagues, who have
been using a tightly focused pressure stimulus applied to cortex, and
then examining the sequelae in deeper structures, especially hippocampus.
Amazingly, there appear to be specific populations of GABAergic
hippocampal interneurons that are selectively damaged by such an insult,
whereas the surrounding cells remain relatively unscathed. Although this
injury does not produce epilepsy, it is intriguing that trauma can have
such specific effects on inhibitory interneurons. 

Also, regarding primed-burst potentiation, I usually think of that as a
"refinement" of LTP. It is possible to elicit LTP (i.e., which I'm
provisionally defining as any potentiation that lasts as long as the
experiment, regardless of mechanism) with primed-burst protocols, which
as you hint are much more likely to be physiologically relevant than
tetanic stimuli. As I understand the original work of Tom Dunwiddie and
subsequent work by others, PBP relies completely on "disinhibition" via
GABA-B receptors.  It's not surprising that there might be differences
between LTP evoked by the traditional "sledgehammer" tetanic protocols
and the that evoked by primed bursts.

Now I'm just waiting for the inevitable posts deriding me for hitting
animals with sledgehammers. 

Cheers,

Matt



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