The data reported provide evidenceto support the concept of a neural regulation of growth hormone (GH) secretion in mammals. Electrolytic lesions in discrete hypothalamic areas result in a reduction of pituitary and plasma radioimmunoassayable (RIA) GH levels and stunting of growth in animals, or impair the acute GH re-sponse to the stimulus of insulin hypoglycemia. Conversely, increases in plasma GH are present after electrical stimulation of brain areas. Hypothalamic regulation of GH secretion would seem to be exerted through a neurohormone designated GH-releasing hormone (GH-RH), which has been characterized by a bioassay system. GH-RH has been purified, isolated, and synthesized and appears to be a straight-chain acidic decapeptide; however, the lack of effect of GH-RH on the release of RIA-GH, either in vitro or in vivo, introduces some elements of uncertainty and the problem is further compounded by contradictions between bioassay and RIA data in the rat. Proof has recently been afforded for the existence of an inhibitory hypothalamic factor (GIF), the physiological significance of which in the control of GH secretion remains to be established. GH-RH decreases in the hypothalamus and increases in the plasma in situations where GH release is enhanced, thus stressing the importance of the neurohormonal mechanism. Pharmacological studies in animals and in humans support the concept that the adrenergic system plays a significant role in the neurohormonal control of GH secretion. Serum GH is acutely increased in humans, following ingestion of L-dopa, an aminoacid precursor of dopamine; conversely, chlorpromazine, an antiadrenergic drug, is effective in depressing GH levels. A pattern of intermittent bursts of GH secretion is present in humans during the time of deeper sleep, apparently independent of alterations in brain catecholamine turnover. Finally, like other anterior pituitary hormones, GH appears to feed back on itself to decrease its own secretion.