Direct evidence for involvement of dopaminergic inhibition and cholinergic activation in yawning.

A behavioral study was performed in an attempt to understand the neurological mechanism involved in yawning in rats. Intraperitoneal injections of low doses (0.25 mg/kg) of apomorphine, which preferentially activate presynaptic dopamine autoreceptors, elicited yawning. Whereas apomorphine, at a high dose of 2 mg/kg, produces stereotypy which has been thought to be mediated by stimulation of postsynaptic dopamine receptors. The yawning and stereotypy did not occur simultaneously in the rat. The apomorphine-induced yawning was completely inhibited by pretreatment with fluphenazine (9 mg/kg, IM) or scopolamine (0.5 mg/kg IP), but markedly increased by reserpine (5 mg/kg, SC), however it was not affected by methylscopolamine (0.5 mg/kg, IP). Both physostigmine (0.2 mg/kg, IP), an indirect acetylcholine agonist, and pilocarpine (4 mg/kg, IP), a direct acetylcholine agonist, also induced yawning. This was abolished by scopolamine (0.5 mg/kg, IP) and increased by reserpine (5 mg/kg, SC). Fluphenazine (9 mg/kg, IP) did not affect the pilocarpine-induced yawning but increased the physostigmine-induced yawning. The results indicate that apomorphine elicits yawning by stimulating presynaptic dopamine receptors, and that dopaminergic inhibition and cholinergic activation are concomitantly involved in the yawning.