Abstract
A micromethod has been used for studying the passage of 36Cl− ions between two microchambers across the GABA acceptive plasma membrane of the rabbit Deiters' neurone, under various different conditions. The presence of 3.3 mM GABA, steady state intracellular concentration in situ (Okada & Shimada, 1976), on the cytoplasmic side of those membranes prolongs remarkably the time for the achievement of 36Cl− equilibrium across the membranes (from 4 minutes to 30 minutes).
The effect appears to be mediated by “intracellularly oriented” GABAA receptor complexes as studied with GABAA antagonists such as bicuculline and picrotoxin. Intracellular GABA is still active in this effect at 10−6 M. This phenomenon is discussed as, when coupled with the intracellular ATP producing machinery, being of importance for synaptically released GABA hyperpolarizing action on these neurones.
The action of intracellular GABA on “internally oriented” receptors appears to involve the exposure of positively charged loci at the cytoplasmic side of the membrane. The consequent accumulation of intracellular Cl− at the membrane inner side would account for the higher overall permeability of those ions in the → out direction. This circustance was assessed by blocking the intracellular GABA effect either working at a relatively basic pH (8.4) inside or increasing the ionic strength in the intracellular compartment.