1. The effects of vasoactive intestinal polypeptide (VIP) on the inferior mesenteric ganglion of the guinea‐pig were studied in vitro. 2. In 67% of the neurones tested, application of VIP (1‐7.5 X 10(‐5) M) by pressure ejection caused a depolarization of the membrane potential which averaged 8.6 +/‐ 0.4 mV. 3. In 52% of the cells that were responsive to VIP, the membrane depolarization was accompanied by a decrease in membrane input resistance. In another 48% of the cells tested, there was an increase in membrane input resistance. 4. Membrane depolarization caused by VIP enhanced the excitability of post‐ganglionic neurones and converted subthreshold electrotonic and subthreshold synaptic potentials to action potentials. 5. The effects of VIP persisted during nicotinic and muscarinic synaptic blockade. The effects of VIP also persisted in a low‐Ca2+, high‐Mg2+ solution. Thus, the site of action of VIP was on the postsynaptic membrane. 6. Electrical stimulation of the lumbar colonic nerves evoked a slow noncholinergic depolarization of the membrane potential. 7. VIP appeared to be one of the transmitters involved in the electrically evoked e.p.s.p. because both prior desensitization with exogenous VIP and VIP antiserum reduced the amplitude of the slow, non‐cholinergic e.p.s.p. 8. Radial distension of a segment of colon attached to the inferior mesenteric ganglion (i.m.g.) evoked a non‐cholinergic depolarization of the membrane potential in neurones in the i.m.g. 9. The distension‐induced non‐cholinergic depolarization was reduced by VIP antiserum. 10. The data support the hypothesis that a population of the mechanosensory afferent nerves running between the colon and the i.m.g. utilize VIP or a VIP‐like peptide as a transmitter to modulate reflex activity between the colon and the i.m.g.
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