MECHANOSENSITIVE CHANNELS TRANSDUCE OSMOSENSITIVITY IN SUPRAOPTIC NEURONS
MECHANOSENSITIVE CHANNELS TRANSDUCE OSMOSENSITIVITY IN SUPRAOPTIC NEURONS
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DOI：
10.1038/364341a0
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发表时间：
1993-07-22
期刊：
影响因子：
64.8
通讯作者：
BOURQUE, CW
中科院分区：
文献类型：
--
作者：
OLIET, SHR;BOURQUE, CW
加压素是由视上核和室旁核的神经元合成的肽激素，其将轴突终末投射到神经垂体。与其抗利尿特性一致，加压素释放作为血浆渗透压的函数而升高1 -3，这是由加速动作电位放电引起的反应4 -6。先前的研究表明，在缺乏突触传递的情况下，液体渗透压的增加使视上神经元退化7 -9，这表明这些细胞表现为内源性β受体。然而，将渗透压摩尔浓度的变化转换为电信号的机制尚不清楚。在这里，我们报告，细胞体积的变化伴随着液体渗透压的生理变化，这些调节的方式是一致的膜电压和动作电位放电的宏观调控的机械敏感性阳离子通道的活性。这些发现定义了哺乳动物中枢神经元中拉伸失活通道的功能。
VASOPRESSIN is a peptide hormone synthesized by neurons of the supraoptic and paraventricular nuclei, which project axon terminals to the neurohypophysis. Consistent with its antidiuretic properties, vasopressin release rises as a function of plasma osmolality1-3, a response that results from accelerated action potential discharge4-6. Previous studies have shown that increases in fluid osmolality depolarize supraoptic neurons in the absence of synaptic transmission7-9, suggesting that these cells behave as intrinsic osmoreceptors. The mechanism by which changes in osmolality are transduced into an electrical signal is unknown, however. Here we report that changes in cell volume accompany physiological variations in fluid osmolality and that these modulate the activity of mechanosensitive cation channels in a way that is consistent with the macroscopic regulation of membrane voltage and action potential discharge. These findings define a function for stretch-inactivated channels in mammalian central neurons.