Sakatani K, Hassan A Z, Chesler M
Department of Neurosurgery, New York University Medical Center, New York 10016.
Exp Neurol. 1994 Jun;127(2):291-7. doi: 10.1006/exnr.1994.1105.
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.
γ-氨基丁酸（GABA）可使大鼠视神经轴突去极化，并通过激活GABA-A受体来调节轴突传导。为了探究细胞外钾离子浓度（[K+]e）升高是否在GABA对大鼠视神经的作用中起主要作用，我们在体外研究了GABA对新生大鼠视神经轴突传导和[K+]e的影响。使用双管钾离子敏感微电极记录[K+]e。GABA（10^-4 - 10^-3 M）可使新生视神经中的[K+]e升高。在长时间应用过程中，[K+]e缓慢恢复。GABA-A受体阻断剂荷包牡丹碱（10^-4 M）可显著降低GABA诱导的[K+]e升高。GABA-A激动剂异鹅去甲肾上腺素（10^-4 M）模拟了GABA的作用，但在相同浓度下产生了更大的反应。相比之下，GABA-B激动剂巴氯芬（10^-4 M）对[K+]e没有影响。GABA诱导的复合动作电位变化仅部分与[K+]e变化相关。此外，钾离子升高诱导的复合动作电位变化远小于GABA诱导的变化。这些结果表明，GABA诱发的[K+]e积累在GABA对新生大鼠视神经的作用中起次要作用。
