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由质膜Ca2+/H+泵介导的海马神经元酸中毒。

Acidosis of hippocampal neurones mediated by a plasmalemmal Ca2+/H+ pump.

作者信息

Trapp S, Lückermann M, Kaila K, Ballanyi K

机构信息

II. Physiologisches Institut, Universität Göttingen, Germany.

出版信息

Neuroreport. 1996 Aug 12;7(12):2000-4. doi: 10.1097/00001756-199608120-00029.

DOI:10.1097/00001756-199608120-00029
PMID:8905712
Abstract

Modulation of cytosolic calcium ([Ca2+]i) plays a key role in intracellular signalling. In neurones, intracellular Ca2+ transients are involved in the regulation of excitability as well as in synaptic transmission and plasticity. Here, we report that depolarization-induced elevation of [Ca2+]i evokes a prominent fall of intracellular pH (pHi) in voltage-clamped hippocampal pyramidal neurones dialysed with fluorescent indicators of H+ and Ca2+. This acidification is caused by exchange of internal calcium for extracellular protons via a vanadate- and eosin-sensitive plasmalemmal Ca2+/H+ pump. In view of the potent neuromodulatory actions of H+, these results raise the possibility that changes in excitability and synaptic plasticity, hitherto solely attributed to Ca2+ transients, may include a significant component mediated by pH shifts.

摘要

胞质钙([Ca2+]i)的调节在细胞内信号传导中起关键作用。在神经元中,细胞内Ca2+瞬变参与兴奋性调节以及突触传递和可塑性。在此,我们报告在用H+和Ca2+荧光指示剂透析的电压钳制海马锥体神经元中,去极化诱导的[Ca2+]i升高会引起细胞内pH(pHi)显著下降。这种酸化是由内部钙通过钒酸盐和曙红敏感的质膜Ca2+/H+泵与细胞外质子交换引起的。鉴于H+具有强大的神经调节作用,这些结果增加了一种可能性,即迄今为止仅归因于Ca2+瞬变的兴奋性和突触可塑性变化可能包括由pH变化介导的重要成分。

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