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在体内注射辣椒素后,哺乳动物肠系膜下神经节中的慢兴奋性突触后电位依然存在。

A slow EPSP in mammalian inferior mesenteric ganglion persists after in vivo capsaicin.

作者信息

Peters S, Kreulen D L

出版信息

Brain Res. 1984 Jun 11;303(1):186-9. doi: 10.1016/0006-8993(84)90227-0.

Abstract

The non-cholinergic slow excitatory postsynaptic potential (EPSP) in the guinea pig inferior mesenteric ganglion (IMG) is believed to be mediated by substance P (SP). Yet, in ganglia of guinea pigs treated with capsaicin (50, 100, or 350 mg/kg, s.c.), a compound that depletes SP from sensory neurons, slow EPSPs were only 50% smaller in amplitude than those in vehicle-treated controls; this was true at all dosages. When ganglia from capsaicin-treated animals were desensitized to SP, slow EPSP amplitude was decreased by 50% from predesensitization values. These data indicate that capsaicin does not eliminate the slow EPSP in the IMG and suggest that both SP and another transmitter are involved in co-mediating this response.

摘要

豚鼠肠系膜下神经节(IMG)中的非胆碱能慢兴奋性突触后电位(EPSP)被认为是由P物质(SP)介导的。然而,在用辣椒素(50、100或350mg/kg,皮下注射)处理的豚鼠神经节中,辣椒素是一种能使感觉神经元中的SP耗竭的化合物,慢EPSP的幅度仅比用赋形剂处理的对照组小50%;所有剂量下均如此。当来自辣椒素处理动物的神经节对SP脱敏后,慢EPSP幅度比脱敏前的值降低了50%。这些数据表明辣椒素并未消除IMG中的慢EPSP,并提示SP和另一种递质共同参与介导这种反应。

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