title: [Ca2+ channels in the central nervous system].
abstract: Roles of Ca2+ channels in physiological functions of mammalian central synapses were discussed from a system-oriented point of view. In the presynaptic terminals of the mammalian CNS so far studied, synaptic transmission is mediated by the subclass of Ca2+ channels designated as the N-type (alpha 1B channels) and/or by that designated as the P/Q-type (alpha 1A channels). In some central synapses such as those between neocortical pyramidal neurons, synaptic transmission is presynaptically suppressed by various transmitter-modulators. Our electrophysiological data indicate that the receptors for amines, glutamate, GABA and adenosine co-exist on individual terminals, and they exert a common modulatory effect on synaptic transmission. Details of the intracellular cascade, i.e., G-protein and Ca2+ channel subtypes that are linked in this modulation, remain to be elucidated. Although the direct 'membrane delimited' action of G-proteins on Ca2+ channels is strongly suggested as a modulatory mechanism by the resemblance to the modulation observed in other neurons, the indirect second messenger pathways, however, may also be involved in the control of Ca2+ channels. Postsynaptically located Ca2+ channels are considered to play important roles in the regulation of neuronal excitability and synaptic plasticity. Individual dendritic spines apparently serve as a primary unit in an increase in Ca2+ level. This compartmentalized increase of Ca2+ seems essential for determining plastic changes of the synaptic efficacy in those particular spines. There is ample evidence indicating that the postsynaptic Ca2+ channels are involved in this Ca2+ transient. In order to understand the physiological significance of Ca2+ channels in CNS functions, further elucidation of channel subtypes, intracellular cascades of the modulator actions and characterization of the channel modifications will be essential.
authors.affiliation: Department of Pharmacology, School of Medicine, Tokyo Medical and Dental University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Murakoshi
authors.forename: T
authors.initials: T
authors.lastname: Tanabe
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology; D015220:Calcium Channels / Q000145:classification / Q000502:physiology*; D002490:Central Nervous System / Q000502:physiology*; D003712:Dendrites / Q000502:physiology; D019204:GTP-Binding Proteins / Q000378:metabolism / Q000502:physiology; D006801:Humans; D009473:Neuronal Plasticity; D018377:Neurotransmitter Agents / Q000502:physiology; D017982:Receptors, Biogenic Amine / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission
chemical_list: D015220:Calcium Channels; D018377:Neurotransmitter Agents; D017982:Receptors, Biogenic Amine; D019204:GTP-Binding Proteins; D002118:Calcium