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γ‐Aminobutyric Acid and Benzodiazepine Binding Sites in Audiogenic Seizure‐Susceptible Mice
Author(s) -
Horton R. W.,
Prestwich S. A.,
Meldrum B. S.
Publication year - 1982
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.1471-4159.1982.tb07972.x
Subject(s) - flunitrazepam , aminobutyric acid , benzodiazepine , medicine , endocrinology , stimulation , gamma aminobutyric acid , chemistry , ratón , biology , receptor
The properties of γ‐aminobutyric acid recognition sites, benzodiazepine binding sites and the effect of exogeneous γ‐aminobutyric acid on benzodiazepine binding were determined in crude membrane fractions prepared from the brains of DBN/2 mice at ages before (8‐9 and 17‐18 days), during (22‐23 and 28‐29 days) and after (40‐43 days) the age of high susceptibility to audiogenic seizures. These have been compared with data from age‐ matched mice of a strain (TO) with lower audiogenic seizure susceptibility. The number of high‐affinity [ 3 H]γ‐aminobutyric acid binding sites was lower at all ages in DBN/2 mice compared with TO mice, but the affinity was higher in DBN/2 mice. The number of low‐affinity [ 3 H]y‐aminobutyric acid binding sites was lower at 8‐9 days and 40‐43 days in DBN/2 mice, but was not significantly different from TO mice at other ages. For [ 3 H]flunitrazepam binding, the only difference found was a slight reduction in the number of binding sites at 28‐29 days of age in DBN/2 mice. γ‐Aminobutyric acid stimulation of [ 3 H]‐flunitrazepam binding was not significantly different up to 22‐23 days of age, but was higher in DBN/2 mice at 28‐29 days and lower at 40‐43 days. Impairment of γ‐aminobutyric acid function is a possible permissive factor in the age‐dependent audiogenic seizure susceptibility in DBN/2 mice.