Presynaptic modulation of cholinergic and non‐cholinergic fast synaptic transmission in the myenteric plexus of guinea pig ileum

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Abstract
Abstract  These studies investigated receptors modulating release of mediators of fast excitatory postsynaptic potentials (fEPSPs) in guinea pig ileum myenteric plexus using electrophysiological methods. Fast EPSPs inhibited by >95% by hexamethonium (100 μmol L−1) were cholinergic; mixed fEPSPs were inhibited 50 = 18 nmol L−1), mixed (81%, 21 nmol L−1) and non‐cholinergic (76%, 44 nmol L−1) fEPSPs equally. The 5‐HT1 receptor agonist 5‐carboxamidotryptamine inhibited cholinergic, mixed and non‐cholinergic fEPSPs equally. Renzapride, increased non‐cholinergic (33%) less than mixed (97%, 13 μmol L−1) fEPSPs. Renzapride inhibited the purely cholinergic fEPSPs (−29%) but potentiated the cholinergic component of mixed fEPSPs (39%). Prucalopride potentiated all fEPSPs equally (30–33%). 5‐HT (0.1 μmol L−1) induced potentiation of cholinergic (75%), mixed (97%) and non‐cholinergic (84%) fEPSPs was not statistically different. The potentiating effects of renzapride and 5‐HT on fEPSPs were inhibited by the 5‐HT4 receptor antagonist, SB 204070 (10 nmol L−1). Renzapride (0.3 μmol L−1) blocked 5‐HT‐induced increases in cholinergic fEPSPs. α2‐Adrenergic and 5‐HT1 receptors mediate inhibition of transmitter release from cholinergic and mixed terminals. 5‐HT and prucalopride, acting at 5‐HT4 receptors, facilitate all fEPSPs; renzapride facilitates the cholinergic and non‐cholinergic components of mixed fEPSPs but not purely cholinergic fEPSPs. Cholinergic synapses may express few 5‐HT4 receptors or a renzapride‐insensitive 5‐HT4 receptor isoform.

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