Asymmetrical activation of GABA-gated chloride channels in cerebral cortex.

Autor: McIntyre TD; Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, MD 20892., Trullas R, Skolnick P
Jazyk: angličtina
Zdroj: Pharmacology, biochemistry, and behavior [Pharmacol Biochem Behav] 1988 Aug; Vol. 30 (4), pp. 911-6.
DOI: 10.1016/0091-3057(88)90119-0
Abstrakt: A pronounced left/right asymmetry of GABA-gated chloride channels was observed in rat cerebral cortex. This asymmetry was manifest as a higher apparent affinity and density of binding sites for the "cage" convulsant [35S]t-butylbicyclophosphorothionate (TBPS) in the right compared to left cortex. Asymmetries in [35S]TBPS binding were not observed in other brain areas, and were restricted to the occipital and entorhinal/pyriform areas of cerebral cortex. Evaluation of other components of the benzodiazepine/GABA receptor chloride ionophore complex in cerebral cortex suggests that this asymmetry is not present in either benzodiazepine receptors or that population of GABA receptors linked to benzodiazepine receptors. Brief restraint-stress significantly increased both the apparent affinity and number of [35S]TBPS binding sites in cortex, but the left/right asymmetry was no longer apparent. These findings indicate a time-dependent, asymmetric response of cortical GABA-gated chloride channels to stress rather than an anatomical hemispheric difference, and suggest that GABA-gated chloride channels may be involved in a differential processing of stressful stimuli by the cerebral hemispheres.
Databáze: MEDLINE