Frings S, Reuter D, Kleene S J
Institut für Biologische Informationsverarbeitung, Forschungszentrum Jülich, Germany.
Prog Neurobiol. 2000 Feb;60(3):247-89. doi: 10.1016/s0301-0082(99)00027-1.
Ca2+ -activated Cl- channels control electrical excitability in various peripheral and central populations of neurons. Ca2+ influx through voltage-gated or ligand-operated channels, as well as Ca2+ release from intracellular stores, have been shown to induce substantial Cl- conductances that determine the response to synaptic input, spike rate, and the receptor current of various kinds of neurons. In some neurons, Ca2+ -activated Cl- channels are localized in the dendritic membrane, and their contribution to signal processing depends on the local Cl- equilibrium potential which may differ considerably from those at the membranes of somata and axons. In olfactory sensory neurons, the channels are expressed in ciliary processes of dendritic endings where they serve to amplify the odor-induced receptor current. Recent biophysical studies of signal transduction in olfactory sensory neurons have yielded some insight into the functional properties of Ca2+ -activated Cl- channels expressed in the chemosensory membrane of these cells. Ion selectivity, channel conductance, and Ca2+ sensitivity have been investigated, and the role of the channels in the generation of receptor currents is well understood. However, further investigation of neuronal Ca2+ -activated Cl- channels will require information about the molecular structure of the channel protein, the regulation of channel activity by cellular signaling pathways, as well as the distribution of channels in different compartments of the neuron. To understand the physiological role of these channels it is also important to know the Cl- equilibrium potential in cells or in distinct cell compartments that express Ca2+ -activated Cl- channels. The state of knowledge about most of these aspects is considerably more advanced in non-neuronal cells, in particular in epithelia and smooth muscle. This review, therefore, collects results both from neuronal and from non-neuronal cells with the intent of facilitating research into Ca2+ -activated Cl- channels and their physiological functions in neurons.
钙离子激活的氯离子通道控制着各种外周和中枢神经元群体的电兴奋性。已表明，通过电压门控或配体门控通道的钙离子内流，以及细胞内储存库释放的钙离子，均可诱导大量的氯离子电导，这些电导决定了对突触输入、放电频率以及各类神经元受体电流的反应。在某些神经元中，钙离子激活的氯离子通道定位于树突膜，它们对信号处理的贡献取决于局部氯离子平衡电位，该电位可能与胞体膜和轴突膜的电位有很大差异。在嗅觉感觉神经元中，这些通道在树突末梢的纤毛突起中表达，在那里它们用于放大气味诱导的受体电流。最近对嗅觉感觉神经元信号转导的生物物理研究，对这些细胞化学感受膜中表达的钙离子激活的氯离子通道的功能特性有了一些了解。已经研究了离子选择性、通道电导和钙离子敏感性，并且对这些通道在受体电流产生中的作用也有了很好的理解。然而，对神经元钙离子激活的氯离子通道的进一步研究将需要有关通道蛋白分子结构、细胞信号通路对通道活性的调节以及通道在神经元不同区室中的分布的信息。为了理解这些通道的生理作用，了解表达钙离子激活的氯离子通道的细胞或不同细胞区室中的氯离子平衡电位也很重要。关于这些方面中大多数的知识状态在非神经元细胞中，特别是在上皮细胞和平滑肌细胞中要先进得多。因此，本综述收集了来自神经元和非神经元细胞的结果，旨在促进对钙离子激活的氯离子通道及其在神经元中的生理功能的研究。
