GABA autoreceptors are not coupled to benzodiazepine receptors in rat cerebral cortex.
Depolarization-induced release of [3H]gamma-aminobutyric acid ([3H]-GABA) from preloaded slices of rat cerebral cortex was inhibited by muscimol and THIP in a dose-dependent fashion. This inhibition of release was prevented by the GABA antagonists bicuculline and picrotoxin. These results confirm previous reports postulating the existence of GABA autoreceptors on GABAergic terminals. Since benzodiazepines are known to facilitate post-synaptic GABA actions, the effect of flunitrazepam on the inhibition of GABA release mediated through the autoreceptors has been examined. At a concentration of 1 microM or 10 microM, flunitrazepam had no effect on the IC50 values for muscimol or THIP in inhibiting stimulated GABA release. It thus seems that GABA autoreceptors are not functionally coupled to benzodiazepine receptors in rat cerebral cortex.[1]References
- GABA autoreceptors are not coupled to benzodiazepine receptors in rat cerebral cortex. Brennan, M.J. J. Neurochem. (1982) [Pubmed]
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