Details

Autor(en) / Beteiligte

• Nanou, Evanthia
• Catterall, William A.

Titel

Calcium Channels, Synaptic Plasticity, and Neuropsychiatric Disease

Ist Teil von

• Neuron (Cambridge, Mass.), 2018-05, Vol.98 (3), p.466-481

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2018

Quelle

EZB-FREE-00999 freely available EZB journals

Beschreibungen/Notizen

• 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. This article reviews advances in understanding structure and regulation of presynaptic and postsynaptic calcium channels and their signaling complexes. Roles of calcium channel regulation in presynaptic and postsynaptic plasticity are presented. Impacts of these processes on neuropsychiatric diseases are discussed.