EFFECTS OF GABA ON AXONAL CONDUCTION AND EXTRACELLULAR POTASSIUM ACTIVITY IN THE NEONATAL RAT OPTIC-NERVE

GABA depolarizes rat optic nerve axons and modulates axonal conduction through the activation of GABA-A receptors. To address whether an increase of [K+](e) plays a major role in GABA actions on the rat optic nerve, we studied the effects of GABA on axonal conduction and [K+](e) in the neonatal rat optic nerve in vitro. Double-barrelled K+-sensitive microelectrodes were used to record [K+](e). GABA (10(-4)-10(-3) M) increased [K+](e) in the neonatal optic nerve. During prolonged application, the [K+](e) slowly recovered. The increase in [K+](e) induced by GABA was markedly reduced by the GABA-A receptor blocker bicuculline (10(-4) M). Isoguvacine (10(-4) M), a GABA-A agonist, mimicked the effect of GABA but produced larger responses at the same concentration. In contrast, baclofen (10(-4) M), a GABA-B agonist, had no effect on [K+](e). The changes in the compound action potential induced by GABA correlated only partially with the [K+](e) changes. Furthermore, the changes in the compound action potential induced by elevation of K+ were far less than those induced by GABA. These results demonstrate that the GABA-evoked accumulation of [K+](e) plays a secondary role in GABA actions on the neonatal rat optic nerve. (C) 1994 Academic Press, Inc.