Inhibitory effect of neuropeptide Y on growth hormone secretion in rats is mediated by both Y1- and Y2-receptor subtypes and abolished after anterolateral deafferentation of the medial basal hypothalamus.

Neuropeptide Y (NPY) may play a physiological role in the regulation of growth hormone (GH) secretion by acting via somatostatin (SS) in the periventricular nucleus (PeV), as well as via the GH-releasing factor in the arcuate nucleus (ARC) of the medial basal hypothalamus (MBH). The objectives of the present study were to determine the neuron structures and receptor subtypes necessary for mediating the inhibitory effect of NPY on GH secretion in unanesthetized male rats. To eliminate the influence of hypophyseotropic SS, anterolateral deafferentation (ALC) of the hypothalamus was performed. Intracerebroventricular (i.c.v.) administration of 1.17 nmol of NPY decreased the blood level of GH for 3-4 h in sham-operated rats, while the procedure was without effect in ALC rats. The i.c.v. administration of 1.17 nmol of a Y1-receptor agonist ([Leu31, Pro34]-NPY) or a Y2-receptor agonist (NPY 13-36 and NPY 3-36) similarly suppressed the blood GH level. The data support the hypothesis that neuron structures anterolateral to the MBH are required for NPY-induced inhibition of GH secretion that is mediated via Y1- and Y2-receptor subtypes. Combined with data of other investigators, SS is likely the neurohumoral mediator of the effect of NPY on GH secretion.