Neuroregulation of growth hormone secretion in domestic animals

Growth hormone (GH) is essential for postnatal somatic growth, maintenance of lean tissue at maturity in domestic animals and milk production in cows. This review focuses on neuroregulation of GH secretion in domestic animals , Two hormones principally regulate the secretion of GH: growth hormone-rel easing hormone (GHRH) stimulates, while somatostatin (SS) inhibits the secr etion of GH. A long-standing hypothesis proposes that alternate secretion o f GHRH and SS regulate episodic secretion of GH, However, measurement of GH RH and SS in hypophysial-portal blood of unanesthetized sheep and swine sho ws that episodic secretion of GHRH and SS do not account for all episodes o f GH secreted. Furthermore, the activity of GHRH and SS neurons decreases a fter steers have eaten a meal offered for a 2-h period each day (meal-feedi ng) and this corresponds with reduced secretion of GH. Together, these data suggest that other factors also regulate the secretion of GH. Several neur otransmitters have been implicated in this regard. Thyrotropin-releasing ho rmone, serotonin and gamma -aminobutyric acid stimulate the secretion of GH at somatotropes. Growth hormone releasing peptide-6 overcomes feeding-indu ced refractoriness of somatotropes to GHRH and stimulates the secretion of GHRH. Norepinephrine reduces the activity of SS neurons and stimulates the secretion of GHRH via alpha (2)-adrenergic receptors. N-methyl-d, 1-asparta te and leptin stimulate the secretion of GHRH, while neuropeptide Y stimula tes the secretion of GHRH and SS. Activation of muscarinic receptors decrea ses the secretion of SS. Dopamine stimulates the secretion of SS via D-1 re ceptors and inhibits the secretion of GH from somatotropes via D-2 receptor s. Thus, many neuroendocrine factors regulate the secretion of GH in livest ock via altering secretion of GHRH and/or SS, communicating between GHRH an d SS neurons, or acting independently at somatotropes to coordinate the sec retion of GH. (C) 2001 Elsevier Science Inc. All rights reserved.