Function and dysfunction of synaptic calcium channels: insights from mouse models

摘要: In the past few years several spontaneous or engineered mouse models with mutations in Ca2+ channel genes have become available, providing a powerful approach to defining function vivo. There been recent advances outlining phenotypes and functional analysis of encoding pore-forming subunits CaV2.1 (P/Q-type), CaV2.2 (N-type) CaV2.3 (R-type) channels, channels involved controlling neurotransmitter release at mammalian synapses. These data indicate that dominant efficient specific role initiating fast synaptic transmission central excitatory synapses vivo, suggest channelopathies are primarily diseases. The different disorders probably arise from disruption neurotransmission brain regions: cortex case migraine, thalamus absence epilepsy cerebellum ataxia.