独立衍生物TN-871对交感神经节突触传递的影响:突触前对神经递质释放的作用。

Y L Shen, K Hirai, Y Katayama
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引用次数: 0

摘要

利用牛蛙交感神经节细胞的细胞内记录来阐明2-正丁基-1-(4-甲基哌嗪基)-5,6-亚甲基二氧二茚的作用HCl (TN-871)对突触传递的影响。在30 nM下,TN-871增强了胆碱能尼古丁快速兴奋性突触后电位(fast EPSPs),而在3微米下,药物可逆地抑制了它们,而不影响乙酰胆碱诱导的去极化。TN-871不影响神经节细胞的主动和被动电特性。定量分析方法应用于0.54 mM Ca2+/7.56 mM Mg2+林格溶液中的快速EPSPs。n -871在30 nM下显著提高了平均量子含量,在3 nM下显著降低了平均量子含量。在300 nM时,TN-871增加或减少了平均量子含量。在检测的浓度下,TN-871没有改变快速epsp的平均量子大小。在0.99 mM Ca2+/4.86 mM Mg2+林格氏溶液中,快速EPSPs不受nicardipine的影响,但在振幅上被omega- concontoxin以浓度依赖的方式抑制。高浓度的n- 871可能会阻断突触前末端对ω -conotoxin敏感的n型钙通道。这些结果表明,TN-871调节神经节前神经末梢的递质释放,但不改变神经节细胞对乙酰胆碱的突触后敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of an indene-derivative, TN-871, on synaptic transmission in a sympathetic ganglion: presynaptic actions on neurotransmitter release.

Intracellular recordings were made from bullfrog sympathetic ganglion cells to elucidate effects of 2-n-butyl-1-(4-methylpiperazinyl)-5,6-methylenedioxyindene.2 HCl (TN-871) on synaptic transmission. TN-871 at 30 nM augmented cholinergic nicotinic fast excitatory postsynaptic potentials (fast EPSPs), whereas the drug at 3 microM reversibly depressed them, without affecting acetylcholine-induced depolarizations. TN-871 did not affect active and passive electrical properties of the ganglion cells. The quantal analysis method was applied to the fast EPSPs in a 0.54 mM Ca2+/7.56 mM Mg2+ Ringer's solution. The mean quantal content was significantly increased by TN-871 at 30 nM but significantly decreased at 3 microM. TN-871 at 300 nM either increased or decreased the mean quantal content. The mean quantal size of the fast EPSPs was not changed by TN-871 at the concentrations examined. Fast EPSPs in a 0.99 mM Ca2+/4.86 mM Mg2+ Ringer's solution were not affected by nicardipine, but were inhibited in amplitude by omega-conotoxin in a concentration-dependent manner. It is likely that TN-871, in high concentrations, might block omega-conotoxin-sensitive N-type calcium channels in the presynaptic terminals. These results indicate that TN-871 modulates transmitter release from preganglionic nerve terminals without changing the postsynaptic sensitivity of the ganglion cells to ACh.

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