Kocsis J D, Honmou O
Department of Neurology, Yale University School of Medicine, New Haven, CT 06516.
Neurosci Lett. 1994 Mar 14;169(1-2):181-4. doi: 10.1016/0304-3940(94)90386-7.
Membrane potential changes of rat neonatal optic nerves were studied in a sucrose-gap chamber. Nipecotic acid (NPA), which blocks uptake and promotes release of GABA, resulted in a bicuculline-sensitive depolarization (3.08 +/- 0.3 mV, n = 5). Pretreatment of the nerves with the anticonvulsant gabapentin (100 microM for 1 h) resulted in a near doubling of the NPA-induced depolarization (6.64 +/- 0.54 mV, n = 5). Gabapentin itself did not alter membrane potential, nor did brief applications of gabapentin enhance the NPA- or GABA-induced depolarization. Thus, gabapentin appears to enhance the releasable pool of GABA in this CNS neural system. These results have implications for the mechanism of the anticonvulsant properties of gabapentin.
在蔗糖间隙室中研究了新生大鼠视神经的膜电位变化。抑制γ-氨基丁酸（GABA）摄取并促进其释放的尼克酸（NPA）导致荷包牡丹碱敏感的去极化（3.08±0.3 mV，n = 5）。用抗惊厥药加巴喷丁（100μM，作用1小时）预处理神经后，NPA诱导的去极化几乎增加了一倍（6.64±0.54 mV，n = 5）。加巴喷丁本身不会改变膜电位，短暂应用加巴喷丁也不会增强NPA或GABA诱导的去极化。因此，加巴喷丁似乎增加了该中枢神经系统神经系统中GABA的可释放池。这些结果对加巴喷丁抗惊厥特性的机制具有启示意义。
