Voltage-gated calcium channels in autonomic neuroeffector transmission

Calcium influx through voltage-gated calcium channels (VGCCs) is required f or neurotransmitter release. Recent research has characterised several phar macologically and electrophysiologically distinct VGCC subtypes, some of wh ich are involved in neurotransmitter release. Transmitter release from auto nomic neurons can be coupled to calcium entry through N-, P/Q- and/or R-typ e VGCCs; the precise combination of VGCC subtypes appears to vary according to the neurotransmitter, tissue and species. L-type channels rarely appear to be important in autonomic neurotransmitter release. There does not appe ar to be a general rule regarding the nature of the VGCCs coupled to releas e of a particular transmitter in different tissues or species. Release of t he same neurotransmitter from different populations of neurons often reveal s a different pattern of involvement of VGCCs. Transmitters released from t he same population of neurons are sometimes coupled to calcium influx throu gh different VGCC subtypes. However, release of transmitters thought to be co-localised within vesicles is coupled to calcium influx through the same VGCCs. The role of VGCC subtypes in transmitter release can be altered by m ode of nerve stimulation. Different VGCC subtypes may be coupled to transmi tter release at low versus high electrical stimulation frequencies, or in r esponse to potassium depolarization or chemical stimulation. In certain dis ease processes, voltage-gated calcium channels on autonomic neurons can be targeted; for example antibodies to P/Q-type VGCCs in Lambert-Eaton myasthe nic syndrome downregulate VGCCs, thereby inhibiting autonomic neuroeffector transmission. (C) 1999 Elsevier Science Ltd. All rights reserved.