pathology of epilepsy

F. Frank LeFever flefever at
Mon Sep 21 21:05:33 EST 1998

Matt (and onlookers)--

Thanks.  Will search out Soltesz (Magyar?).  Some people at Medical
College of Virginia have been working quietly away at stuff I consider
very important.  With sagittal rather than medial fluid percussion they
can get, depending on degree of impact, selective slight hippocampal
damage OR no histologically observable damage but with longterm
behavioral/cognitive effects.  I believe they have looked at GABA
changes, but much of their work has focused on cholinergic changes.
Lyeth and Hamm are two names that come to mind.

re your Kapur and MacDonald reference: must be VERY recent; OVID disk
Medline search failed to locate it.


In <6u60if$6ie$1 at> Matt Jones <jonesmat at>
>In article <6u0i74$6ev at> F. Frank LeFever,
>flefever at 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
>been using a tightly focused pressure stimulus applied to cortex, and
>then examining the sequelae in deeper structures, especially
>Amazingly, there appear to be specific populations of GABAergic
>hippocampal interneurons that are selectively damaged by such an
>whereas the surrounding cells remain relatively unscathed. Although
>injury does not produce epilepsy, it is intriguing that trauma can
>such specific effects on inhibitory interneurons. 
>Also, regarding primed-burst potentiation, I usually think of that as
>"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,
>as you hint are much more likely to be physiologically relevant than
>tetanic stimuli. As I understand the original work of Tom Dunwiddie
>subsequent work by others, PBP relies completely on "disinhibition"
>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. 

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