Sitges M, Chiu L M, González L
División de Investigaciones Clínicas, Instituto Mexicano de Psiquiatría, SSA, D.F., México.
Neurochem Res. 1993 Oct;18(10):1081-7. doi: 10.1007/BF00966688.
The Ca(2+)-dependent, presumably exocytotic fraction of the [3H]GABA released by depolarization is dissected from the depolarization-induced Na(+)-dependent, carrier-mediated fraction of [3H]GABA release in mouse brain synaptosomes. GABA homoexchange is prevented by the [3H]GABA carrier blocker, DABA. The absence of external Na+ completely abolishes the release of the carrier-mediated, presumably cytoplasmic release of [3H]GABA induced by homoexchange and heteroexchange with GABA and DABA, respectively. The carrier-mediated, Na(+)-dependent fraction of the depolarization-induced release of [3H]GABA is resistant to tetrodotoxin (TTX) but is sensitive to amiloride and verapamil. The Ca(2+)-dependent fraction of the [3H]GABA released by high K+ depolarization is also completely abolished by amiloride (from 300 microM) and sensitive to verapamil (30 microM), but in contrast is insensitive to the absence of external Na+ and to DABA. On the basis of these results we conclude that amiloride and verapamil inhibit high K(+)-induced release of [3H]GABA by antagonizing the entrance of Ca2+ (and possibly Na+ when external Ca2+ is absent) through a population of voltage sensitive presynaptic Ca2+ channels activated by depolarization.
在小鼠脑突触体中，通过去极化释放的[3H]GABA的钙依赖性（推测为胞吐性）部分与去极化诱导的钠依赖性、载体介导的[3H]GABA释放部分区分开来。[3H]GABA载体阻滞剂DABA可阻止GABA同源交换。外部Na+的缺失完全消除了分别由与GABA和DABA的同源交换和异源交换诱导的载体介导的、推测为细胞质的[3H]GABA释放。去极化诱导的[3H]GABA释放中载体介导的、钠依赖性部分对河豚毒素（TTX）有抗性，但对氨氯吡脒和维拉帕米敏感。高钾去极化释放的[3H]GABA的钙依赖性部分也被氨氯吡脒（从300微摩尔）完全消除，对维拉帕米（30微摩尔）敏感，但与外部Na+的缺失和DABA相反，对其不敏感。基于这些结果，我们得出结论，氨氯吡脒和维拉帕米通过拮抗Ca2+（以及在没有外部Ca2+时可能还有Na+）通过一群由去极化激活的电压敏感突触前Ca2+通道的进入来抑制高钾诱导的[3H]GABA释放。
