Cholecystokinin octapeptide depolarizes guinea pig inferior mesenteric ganglion cells and facilitates nicotinic transmission.
Cholecystokinin octapeptide (CCK-8) applied either by superfusion (0.1-10 microM) or by pressure ejection elicited a slow depolarization in a portion of inferior mesenteric ganglion cells studied in vitro. The depolarization which persisted in a low Ca2+/high Mg2+ solution, or solution containing cholinergic antagonists, was often associated with a small to moderate increase in neuronal input resistance, and the response was reduced by conditioning hyperpolarization. Nicotinic excitatory postsynaptic potentials were consistently augmented during the course of CCK-8-induced depolarization. Our results, together with findings of the presence of CCK-immunoreactive fibers in the prevertebral ganglia, suggest that the peptide may serve to facilitate nicotinic transmission.
D000818:Animals; D005071:Evoked Potentials / Q000187:drug effects; D005728:Ganglia, Sympathetic / Q000187:drug effects* / Q000502:physiology; D005731:Ganglionic Stimulants / Q000494:pharmacology*; D006168:Guinea Pigs; D007478:Iontophoresis; D008564:Membrane Potentials / Q000187:drug effects*; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D012844:Sincalide / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects*
D005731:Ganglionic Stimulants; D012844:Sincalide