Lundy P M, Frew R, Fuller T W, Hamilton M G
Biomedical Defence Section, Defence Research Establishment Suffield, Ralston, Alberta, Canada.
Eur J Pharmacol. 1991 Jan 25;206(1):61-8. doi: 10.1016/0922-4106(91)90147-a.
Inactivation of N-type voltage-sensitive Ca2+ channels (VSCC) with omega-conotoxin (omega-CgTx) in tissue obtained from chicken brain produces a concentration dependent (0.01-0.1 microM) inhibition of K(+)-stimulated Ca2+ influx (delta K+), the rise in [Ca2+]i and acetylcholine (ACh) release. In identical preparations from rat brain, Ca2+ influx and the rise in [Ca2+]i were only marginally affected by much higher (1-10 microM) concentrations of omega-CgTx. The release of ACh, however, was inhibited to the same degree with similar amounts of omega-CgTx as those used in chicken brain. An L-type VSCC inhibitor failed to affect any of these parameters alone, or to augment the effect of omega-CgTx. The results suggest that almost all the VSCC in chicken brain are of the N type and that these channels regulate neurotransmitter release. In rat brain, on the other hand, Ca2+ channels resistant to N- or L-type blockers account for almost 75% of the measurable Ca2+ influx and rise in [Ca2+]i. The conspicuous dissociation between the regulation of Ca2+ influx and ACh release demonstrated in rat brain by using omega-CgTx, suggest that neurotransmitter release is governed by only a small proportion of strategically located N-type, omega-CgTx sensitive, VSCC in the presynaptic terminal.
用ω-芋螺毒素（ω-CgTx）使取自鸡脑的组织中的N型电压敏感性钙通道（VSCC）失活，会产生浓度依赖性（0.01 - 0.1微摩尔）地抑制钾离子刺激的钙内流（δK+）、细胞内钙离子浓度（[Ca2+]i）升高以及乙酰胆碱（ACh）释放。在取自大鼠脑的相同制剂中，钙内流和[Ca2+]i升高仅受到高得多（1 - 10微摩尔）浓度的ω-CgTx的轻微影响。然而，ACh的释放受到与鸡脑中使用的相似量的ω-CgTx相同程度的抑制。一种L型VSCC抑制剂单独未能影响这些参数中的任何一个，也未能增强ω-CgTx的作用。结果表明，鸡脑中几乎所有的VSCC都是N型，并且这些通道调节神经递质释放。另一方面，在大鼠脑中，对N型或L型阻滞剂有抗性的钙通道占可测量的钙内流和[Ca2+]i升高的近75%。在大鼠脑中使用ω-CgTx所显示的钙内流调节与ACh释放之间的明显解离表明，神经递质释放仅由突触前终末中一小部分位于关键位置的、对ω-CgTx敏感的N型VSCC控制。
