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首页> 外文期刊>Neuron >Calcium Channels, Synaptic Plasticity, and Neuropsychiatric Disease
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Calcium Channels, Synaptic Plasticity, and Neuropsychiatric Disease

机译：钙通道，突触可塑性和神经精神病疾病

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摘要

Voltage-gated calcium channels couple depolarization of the cell-surface membrane to entry of calcium, which triggers secretion, contraction, neurotransmission, gene expression, and other physiological responses. They are encoded by ten genes, which generate three voltage-gated calcium channel subfamilies: CaV1; CaV2; and CaV3. At synapses, CaV2 channels form large signaling complexes in the presynaptic nerve terminal, which are responsible for the calcium entry that triggers neurotransmitter release and short-term presynaptic plasticity. CaV1 channels form signaling complexes in postsynaptic dendrites and dendritic spines, where their calcium entry induces long-term potentiation. These calcium channels are the targets of mutations and polymorphisms that alter their function and/or regulation and cause neuropsychiatric diseases, including migraine headache, cerebellar ataxia, autism, schizophrenia, bipolar disorder, and depression. This?article reviews the molecular properties of calcium channels, considers their multiple roles in synaptic plasticity, and discusses their potential involvement in this wide range of neuropsychiatric diseases.
机译：电压门控钙通道将细胞表面膜的耦合到进入钙的进入，这触发分泌，收缩，神经递血，基因表达和其他生理反应。它们由十个基因编码，该基因产生三个电压门控钙通道亚壳：Cav1; CAV2;和cav3。在突触中，CAV2通道在突触前神经末端形成大的信号络合物，这对钙入口负责触发神经递质释放和短期突触图塑性的钙入口。 CAV1通道在突触后树突和树突刺形成信号络合物，其钙入口诱导长期增强。这些钙通道是突变和多态性的靶向，其改变其功能和/或调节，导致神经精神疾病，包括偏头痛性头痛，小脑共济失障，自闭症，精神分裂症，双相障碍和抑郁症。这篇文章综述了钙通道的分子特性，考虑了它们在突触塑性中的多种作用，并探讨了它们对这种广泛的神经精神疾病的潜在参与。

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