Either muscarinic or nicotinic cholinergic activation of the medial pontine reticular formation evokes a behavioral state, indistinguishable in most respects from that of natural rapid eye movement sleep. However, the presence of physiologically relevant nicotonic receptors has not been described. Intracellular current and single electrode voltage clamp recordings were used to analyse the electrophysiological responses of rat medial pontine reticular formation neurons to nicotinic activation in vitro. In response to the nicotoinic agonist, 1,1-dimethyl-4-phenylpiperazinium iodine, depolarization in association with an inward current was observed in 70% of the medial pontine reticular formation neurons. This effect was insensitive to the muscarinic antagonist atropine and the nicotinic ganglionic antagonists mecamylamine and hexamethonium. However, the neuromuscular nicotinic antagonist d-tubocurare and dihydro-β-erythroidine were effective. This is consistent with a cholinergic activation of medial pontine reticular formation neurons evoking a rapid eye movement sleep-like behavioral state, at least in part, by nicotinic receptors on these neurons.
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