Stress‐protective Action of β‐Phenyl(GABA): Involvement of Central and Peripheral Type Benzodiazepine Binding Sites

Publisher Website
Google Scholar
Abstract
Forced swimming stress caused a significant increase in the density of central type benzodiazepine binding sites in rat cerebral cortex and hippocampus. The number of peripheral type benzodiazepine binding sites was also enhanced on blood platelets. The affinity of neither central nor peripheral type benzodiazepine binding sites was changed considerably after swimming stress. Pretreatment of rats with β‐(phenyl)GABA (100 mg/kg), a GABABagonist, almost completely eliminated the described changes of the both types of benzodiazepine binding sites caused by swimming stress. In an elevated plus‐maze model of anxiety β‐(phenyl)GABA itself was inactive but like diazepam effectively counteracted the behavioural effects of DMCM, a β‐carboline derivative with anxiogenic properties. The possible involvement of benzodiazepine receptors in the mechanism of action of β‐(phenyl)GABA is discussed.