Delta-opioid receptors mediate inhibition of fast excitatory postsynaptic potentials in cat parasympathetic colonic ganglia.

1 The effects of opioids on synaptic transmission in cat sacral parasympathetic colonic ganglia were studied in vitro, using intracellular electrophysiological techniques. Electrical stimulation of the pelvic nerve evoked fast excitatory postsynaptic potentials (e.p.s.ps), which were blocked by hexamethonium and tetrodotoxin. 2 [D-Pen2, D-Pen5] enkephalin and [Met5]enkephalinamide, delta-opioid receptor agonists, caused concentration-dependent, reversible depression of fast e.p.s.ps, but had no effect on depolarizations evoked by pressure ejection of the nicotinic agonist 1,1-dimethyl-4-phenyl-piperazinium. Cell transmembrane potential and membrane input resistance were also unaffected. 3 U-50,488H, a kappa-opioid receptor agonist, had a very small depressant action while [D-Ala2, MePhe4, Gly-ol5] enkephalin, a mu-opioid receptor agonist, had no effect on fast e.p.s.p. amplitude. Neither compound affected cell transmembrane potential or membrane input resistance. 4 The inhibitory actions of [D-Pen2, D-Pen5] enkephalin were antagonized by both naloxone, an antagonist at each of the three opioid receptor types, and by ICI 174,864, an antagonist selective for delta-opioid receptors. 5 Naloxone and ICI 174,864 both also potentiated fast e.p.s.p. amplitude per se in 50% of cells tested. 6 It is concluded that exogenous opioids act at presynaptic delta-opioid receptors to inhibit sacral parasympathetic synaptic transmission in cat colonic ganglia in vitro. Furthermore, the effects of opioid antagonists alone, suggest that endogenous opioids may also be released by preganglionic nerve stimulation and so regulate the release of acetylcholine in these ganglia.