title: omega-Conotoxin-GVIA-sensitive calcium channels on preganglionic nerve terminals in mouse pelvic and celiac ganglia.
abstract: Release of acetylcholine (ACh) from preganglionic nerve terminals requires calcium entry through voltage-gated 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 omega- 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, omega- 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.
authors.affiliation: School of Biomedical Sciences, Faculty of Health, The University of Newcastle, Callaghan, NSW 2308, Australia. phillip.jobling@newcastle.edu.au
authors.forename: Phillip
authors.initials: P
authors.lastname: Jobling
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001339:Autonomic Fibers, Preganglionic / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D020864:Calcium Channels, N-Type / Q000502:physiology*; D020865:Calcium Channels, P-Type / Q000187:drug effects / Q000502:physiology; D020908:Calcium Channels, R-Type / Q000187:drug effects / Q000502:physiology; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005728:Ganglia, Sympathetic / Q000187:drug effects* / Q000502:physiology; D007001:Hypogastric Plexus / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018408:Patch-Clamp Techniques; D013111:Spider Venoms / Q000494:pharmacology; D013153:Splanchnic Nerves / Q000502:physiology; D020867:omega-Agatoxin IVA / Q000494:pharmacology; D020866:omega-Conotoxin GVIA / Q000494:pharmacology*
chemical_list: D002121:Calcium Channel Blockers; D020864:Calcium Channels, N-Type; D020865:Calcium Channels, P-Type; D020908:Calcium Channels, R-Type; C115521:SNX 482; D013111:Spider Venoms; D020867:omega-Agatoxin IVA; D020866:omega-Conotoxin GVIA; D000109:Acetylcholine