Abstract |
Amygdala-kindled seizures reduced significantly the total number of [3H] quinuclidinyl benzilate binding sites in both dentate and hippocampal gyri compared to electrode implanted unstimulated controls. Both high and low affinity carbachol displaceable binding site populations were significantly reduced in hippocampal gyrus. By contrast, a selective decline of low affinity sites was found in dentate gyrus membranes. The selectivity of the decline in dentate but not hippocampus gyrus underscores the specificity of this molecular response to amygdala-kindled seizures. We suggest that these receptor alterations underlie adaptive mechanisms which antagonize kindled epileptogenesis.
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Authors | D D Savage, J O McNamara |
Journal | The Journal of pharmacology and experimental therapeutics
(J Pharmacol Exp Ther)
Vol. 222
Issue 3
Pg. 670-3
(Sep 1982)
ISSN: 0022-3565 [Print] United States |
PMID | 7108770
(Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Quinuclidines
- Receptors, Muscarinic
- Tritium
- Quinuclidinyl Benzilate
- Carbachol
|
Topics |
- Animals
- Binding Sites
- Carbachol
(pharmacology)
- Hippocampus
(metabolism)
- Kindling, Neurologic
- Male
- Quinuclidines
(metabolism)
- Quinuclidinyl Benzilate
(metabolism)
- Rats
- Rats, Inbred Strains
- Receptors, Muscarinic
(drug effects, metabolism)
- Seizures
(metabolism)
- Tritium
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