2001 Volume 42 Issue 4 Pages 235-241
The calcium ion influx through voltage-dependent calcium channels (VDCCs) has a vital role in the control of neurotransmitter release and membrane excitability. Prepulse facilitation is a phenomenon in which a strong depolarizing pulse induces a form of the VDCCs that exhibits an increased opening probability in response to a given test potential; this persists for several seconds after repolarization. It has been reported that prepulse facilitation occurs via dissociation of the guanosine triphosphate (GTP)-binding proteins (G-proteins) from the VDCCs and that recovery from facilitation involves rebinding of the G-proteins. The heterotrimeric G-proteins act as switches that regulate information processing circuits connecting cell surface G-protein-coupled-receptors to a variety of effectors. In this study, we have studied the characterization of G-protein subtypes in prepulse facilitation of VDCCs currents (ICa) in hamster submandibular ganglion (SMG) neurons, using whole-cell patch clamp recordings. Under control conditions, with GTP (0.1mM) in the recording pipette, the rate of prepulse facilitation was 19.0±1.9% (n=13). Intracellular dialysis with GDP-β-S (0.1mM), G-protein blocker, and pretreatment of neurons with N-ethylmaleimide (NEM) (100μM for 2min), Gi/o blocker, attenuated the rate of prepulse facilitation. Intracellular dialysis of anti-Gq/11-antibody did not alter it. These results suggest that prepulse facilitation of VDCCs is due to Gi/o-types of G-protein, but not to the Gq/11-type, in SMG neurons.
