Release of acetylcholine (ACh) from preganglionic nerve terminals requires calcium entry through voltagegated calcium channels. The calcium channel subtype required for ACh release varies depending on the particular ganglionic synapse. I have investigated the functional role of calcium channels in transmitter release from parasympathetic and sympathetic preganglionic terminals in pelvic and celiac ganglia of female mice. Single electrode voltage clamp was used to measure EPSC amplitude in the absence and presence of selective calcium channel antagonists. In pelvic ganglia ω-conotoxin GVIA, a selective N-type calcium channel antagonist, reduced the amplitude of EPSCs evoked by pelvic nerve stimulation by 46±5% (n=8, P=0.015). In contrast, in the celiac ganglion, ω- conotoxin GVIA had no effect on the amplitude of EPSCs evoked by splanchnic nerve stimulation (P=0.09, n=7). EPSCs in both pelvic and celiac ganglia were resistant to the P-type calcium channel antagonist agatoxin (50 nM, n=5 for both ganglia) and the R-type calcium channel antagonist SNX482 (100 nM, n=4 for both ganglia). These results indicate that in female mice, release of ACh in sympathetic pathways to prevertebral ganglia does not require calcium entry from N-type calcium channels. However, release of ACh from sacral parasympathetic preganglionic neurons requires calcium entry from both N-type and toxin-resistant calcium channels.
Autonomic Neuroscience: Basic and Clinical Vol. 146, Issue 1-2, p. 56-61