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去甲肾上腺素通过α1受体介导的Ca2+信号通路激活血管加压素神经元。

Noradrenaline activates vasopressin neurons via alpha1-receptor-mediated Ca2+ signaling pathway.

作者信息

Shioda S, Yada T, Muroya S, Takigawa M, Nakai Y

机构信息

Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan.

出版信息

Neurosci Lett. 1997 May 2;226(3):210-2. doi: 10.1016/s0304-3940(97)00275-9.

Abstract

Noradrenaline (NA) (1-10 microM), dibutyryl-cAMP (1-5 mM), and forskolin (10-20 microM) increased cytosolic Ca2+ concentration ([Ca2+]i) in isolated arginine-vasopressin (AVP)-containing neurons in the hypothalamic supraoptic nucleus (SON). The NA-induced increase in [Ca2+]i in AVP-containing neurons was abolished by a specific alpha1-antagonist, prazosin (1 microM) and was markedly reduced when treated with a protein kinase A (PKA) blocker, H89 (40 microM). The NA-induced [Ca2+]i was not altered by a protein kinase C (PKC) inhibitor, calphostin C (0.1 microM) and a PKC activator, TPA (100 nM). In general, NA, a known neurotransmitter in the SON, activates AVP-containing neurons via alpha1-receptor which is linked to stimulation of cAMP-PKA-regulated Ca2+ signaling pathway.

摘要

去甲肾上腺素(NA)(1 - 10微摩尔)、二丁酰环磷腺苷(dbcAMP)(1 - 5毫摩尔)和福斯高林(10 - 20微摩尔)可增加下丘脑视上核(SON)中分离出的含精氨酸血管加压素(AVP)的神经元的胞质钙离子浓度([Ca2+]i)。含AVP的神经元中,NA诱导的[Ca2+]i增加被特异性α1拮抗剂哌唑嗪(1微摩尔)消除,并用蛋白激酶A(PKA)阻滞剂H89(40微摩尔)处理时显著降低。NA诱导的[Ca2+]i不受蛋白激酶C(PKC)抑制剂钙磷蛋白C(0.1微摩尔)和PKC激活剂佛波酯(TPA)(100纳摩尔)的影响。一般来说,NA是SON中一种已知的神经递质,它通过与cAMP - PKA调节的Ca2+信号通路刺激相关的α1受体激活含AVP的神经元。

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