During suckling, anaesthetized lactating rats release regular (about every 7 min) but brief )ulses of oxytocin (0·5–1·0 mu.) which produce single transient increases in intramammary [unk]ressure. Drugs which selectively impair synaptic transmission were used to determine the [unk]ole of dopamine and noradrenaline in regulating this natural reflex. Diethyldithiocarbamate 100–200 mg/kg, i.v.) and α-methylparatyrosine (100–400 mg/kg, i.v.) which inhibit the [unk]ynthesis of catecholamines both blocked the suckling-induced release of oxytocin. The milk[unk]jection reflex was also inhibited in a dose-dependent manner by the intravenous administraion of the dopamine antagonists, fluphenazine (0·7 mg/kg), pimozide (1·4 mg/kg), cis-lupenthixol (4·5 mg/kg) and metoclopramide (6·0 mg/kg), and caused a significant inhibition P < 0·01) of the reflex in 50% of the rats tested. The α-adrenoceptor antagonist phenoxy[unk]enzamine (1·4 mg/kg) was similarly effective. Dopamine (40 μg), bromocriptine (10 μg), [unk]pomorphine (100 μg), noradrenaline (10 μg) and phenylephrine (2 μg) injected into the;erebral ventricles evoked a sustained release of oxytocin which produced multiple increases n intramammary pressure; isoprenaline (4 μg) was ineffective. The release of oxytocin evoked [unk]y dopamine and noradrenaline was prevented by cis-flupenthixol and phenoxybenzamine respectively. None of the drugs used affected the mammary sensitivity to exogenous oxytocin lor were their actions modified by pretreatment with propranolol (1 mg/kg). The results [unk]uggest that the neural pathway for the reflex release of oxytocin during suckling in the rat [unk]ontains both dopaminergic and noradrenergic synapses, the latter acting through α-[unk]drenoceptors and being distal in the pathway to the dopaminergic component.