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.