| pubmed-article:8033969 | pubmed:abstractText | 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. | lld:pubmed |
