The role of muscarinic cholinergic mechanisms in the brainstem in the control of oesophageal peristalsis was investigated in rats anaesthetized with urethane. Primary deglutitive peristalsis, evoked by electrical stimulation of the brainstem or intravenous administration of the serotonin agonist quipazine, was abolished for periods of 1.5 to 2 h by scopolamine and atropine (0.1-0.2 microM/kg) as well as by methscopolamine (1.25-5 microM/kg). In contrast, the buccopharyngeal stage of evoked swallowing was facilitated. A deglutitive effector area was mapped in the intermediolateral portion of the solitary complex by the use of micropneumophoretic application of S-glutamate (35-350 pM) and the cholinoceptor agonists D,L-muscarine and acetylcholine (50-100 pM). Scopolamine partially antagonized single propulsive contractions of the oesophagus evoked by S-glutamate, but completely inhibited rhythmic propulsive or synchronous oesophageal contractions evoked by muscarinic agonists or acetylcholine. Injection of S-glutamate or acetylcholine into the ambiguus complex produced propulsive or non-propulsive oesophageal responses depending on location. Responses evoked by acetylcholine were potentiated by systemic administration of physostigmine, but were resistant to scopolamine; propulsive responses evoked by S-glutamate were partially inhibited by scopolamine. Injection of the retrogradely-transported fluorescent tracer bisbenzimide into the rostral ambiguus complex resulted in labelling of a discrete cell group located within the deglutitive region of the solitary complex. It is concluded that this region contains premotor elements forming part of the internuncial network organizing oesophageal peristalsis. The source of postulated cholinergic afferents to these neurones remains to be identified.