Inhibitory synaptic potentials resulting from alpha 2‐adrenoceptor activation in guinea‐pig submucous plexus neurones.

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Abstract
Intracellular recordings were obtained from neurons of the guinea-pig submucous plexus. Inhibitory synaptic potentials (i.p.s.p.) were compared with hyperpolarizations evoked by brief, local applications of noradrenaline [norepinephrine, NE] and by superfusion with adrenoceptor agonists. Hyperpolarizing potentials elicited by brief applications of NE were similar to the i.p.s.p. in latency of onset, amplitude, time course, conductance increase, reversal potential and ionic dependence. Both responses were blocked by low concentrations of Ba2+ and quinine. 6-Hydroxydopamine selectively and irreversibly abolished the i.p.s.p. and resulted in a complete loss of catecholamine fluorescent nerve fibers in the submucous plexus. The .alpha.2-adrenoceptor antagonists, phentolamine, yohimbine and RX781094 [idazoxan], reversibly blocked the i.p.s.p. and the NE hyperpolarization. Prazosin, propranolol, atropine and naloxone had no effect on these responses. Superfusion with NE and clonidine produced dose-dependent membrane hyperpolarizations. NE and clonidine dose-hyperpolarization curves were shifted to the right in a parallel fashion by .alpha.2-adrenoceptor antagonists. Determination of the dissociation equilibrium constants for phentolamine, yohimbine and RX781094 showed that the hyperpolarization produced by NE perfusion is due to .alpha.2-adrenoceptor activation. The release of NE from sympathetic nerves activates post-synaptic .alpha.2-adrenoceptors, resulting in the K+ conductance increase which underlies the i.p.s.p. in submucous plexus neurons.