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嗅觉神经元中的钙信号传导与调节

Calcium signalling and regulation in olfactory neurons.

作者信息

Menini A

机构信息

Istituto di Cibernetica e Biofisica, Consiglio Nazionale delle Ricerche, Via De Marini 6, 16149, Genova, Italy.

出版信息

Curr Opin Neurobiol. 1999 Aug;9(4):419-26. doi: 10.1016/S0959-4388(99)80063-4.

DOI:10.1016/S0959-4388(99)80063-4
PMID:10448159
Abstract

The odorant-induced Ca(2+) increase inside the cilia of vertebrate olfactory sensory neurons controls both excitation and adaptation. The increase in the internal concentration of Ca(2+) in the cilia has recently been visualized directly and has been attributed to Ca(2+) entry through cAMP-gated channels. These recent results have made it possible to further characterize Ca(2+)'s activities in olfactory neurons. Ca(2+) exerts its excitatory role by directly activating Cl(-) channels. Given the unusually high concentration of ciliary Cl(-), Ca(2+)'s activation of Cl(-) channels causes an efflux of Cl(-) from the cilia, contributing high-gain and low-noise amplification to the olfactory neuron depolarization. Moreover, in combination with calmodulin, Ca(2+) mediates odorant adaptation by desensitizing cAMP-gated channels. The restoration of the Ca(2+) concentration to basal levels occurs via a Na(+)/Ca(2+) exchanger, which extrudes Ca(2+) from the olfactory cilia.

摘要

脊椎动物嗅觉感觉神经元纤毛内气味剂诱导的Ca(2+)增加控制着兴奋和适应过程。最近已直接观察到纤毛内Ca(2+)的内部浓度增加,这归因于Ca(2+)通过cAMP门控通道的进入。这些最新结果使得进一步表征Ca(2+)在嗅觉神经元中的活动成为可能。Ca(2+)通过直接激活Cl(-)通道发挥其兴奋作用。鉴于纤毛中Cl(-)浓度异常高,Ca(2+)对Cl(-)通道的激活导致Cl(-)从纤毛流出,为嗅觉神经元去极化提供高增益和低噪声放大。此外,Ca(2+)与钙调蛋白结合,通过使cAMP门控通道脱敏来介导气味剂适应。Ca(2+)浓度恢复到基础水平是通过Na(+)/Ca(2+)交换器实现的,该交换器将Ca(2+)从嗅觉纤毛中挤出。

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