In adult rats, the noradrenergic system plays a role in pulsatile and opiate-stimulated growth hormone (GH) secretion through stimulation of alpha-2 adrenergic receptors. The present studies examine catecholaminergic mechanisms which might regulate GH release in the neonatal rat. Catecholaminergic involvement in opiate-induced GH secretion was examined in 10-day-old and 30-day-old rats. Rats were sacrificed 30 min after administration of methadone (2.5 mg/kg s.c.) and serum was analyzed for GH by radioimmunoassay. Reserpine (1 mg/kg s.c.) abolished methadone-induced GH release in neonatal rats. Haloperidol (1 mg/kg s.c.) but not cyproheptadine (5 mg/kg i.p.) attenuated methadone-stimulated GH release. The role of noradrenergic neurons in opiate-induced GH secretion was examined by pretreating rats with diethyldithiocarbamate (400 mg/kg i.p.) or phenoxybenzamine (10 mg/kg i.p.). Both treatments blocked methadone-induced GH release in neonatal rats. In 30-day-old rats, pretreatment with yohimbine (2.5 mg/kg i.p.), but not prazosin (2.5 mg/kg s.c.) blocked opiate-induced GH release. Although selective blockade by these alpha-1 and alpha-2 antagonists could not be demonstrated in neonatal rats, the alpha-2 agonist, clonidine, did stimulate GH release in a dose-related manner. Findings suggest that noradrenergic mechanisms participate in the regulation of GH secretion in both neonatal and adult rats. A tonically active alpha-2 system is demonstrable in neonates despite the absence of GH surges. The GH response to opiates appears to be mediated through this mechanism. Neural regulation of surging may develop as a separate pathway or become superimposed on the neonatal circuit.