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Postnatal Evolution of the γ‐Aminobutyric Acid/Benzodiazepine Receptor Complex in a Model of Inherited Epilepsy: The Quaking Mouse
Author(s) -
Caboche Jocelyne,
Mitrovic Nadia,
Le Saux Françoise,
Besson MarieJo,
Sauter André,
Maurin Yves
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb09137.x
Subject(s) - gabab receptor , muscimol , baclofen , gabaa receptor , agonist , forebrain , gabaergic , flunitrazepam , gamma aminobutyric acid , benzodiazepine , mutant , zolpidem , cerebellum , biology , diazepam , endocrinology , epilepsy , medicine , receptor , pharmacology , neuroscience , biochemistry , central nervous system , gene , insomnia
Binding assays of [ 3 H]muscimol and [ 3 H]‐flunitrazepam have been performed on brain homogenates of brainstem, cerebellum, and forebrain of genetically epileptic quaking ( qk ) mutant mice 20, 40, 70, and 90 days old and their corresponding controls of the same strain (C57BL/ 6J). The endogenous γ‐aminobutyric acid (GABA) content has been determined in various brain regions of 70‐day‐old qk and control mice. Finally, the behavioral effects of diazepam, of the mixed GABA A /GABA B receptor agonist progabide, and of the selective GABA B receptor agonist baclofen have been assessed in adult qk mutants. Our results strongly suggest a lack of involvement of GABAergic neurotransmission in the inherited epilepsy of the qk mutant mouse.