Somatostatin inhibits alpha-2-adrenergic-induced secretion of growth hormone-releasing hormone

The purpose of this experiment waste determine the role of growth hormone-r eleasing hormone (GHRH) and somatostatin (SRIH) neurons in mediating alpha (2)-adrenergic receptor-induced stimulation of growth hormone (GH) secretio n in cattle. Our first objective was to determine if stimulation of alpha ( 2)-adrenergic receptors increases activity of GHRH neurons in the arcuate n ucleus (ARC) and/or decreases activity of SRIH neurons in periventricular ( PeVN) and ARC nuclei. Clonidine tan alpha (2)-adrenergic agonist) or vehicl e (saline) were injected i.v, into steers and dual-label immunohistochemist ry was performed to quantify the number of GHRH and SRIH neurons expressing Fos and Fos-related antigens (Fos/FRA) as markers of neuronal activity. Cl onidine increased concentrations of GH in serum and decreased activity of S RIH neurons in the PeVN, but not in the ARC. Clonidine did not alter activi ty of GHRH neurons in the ARC. Our second objective was to determine if clo nidine de creases secretion of SRIH from perifused slices of hypothalami, w hich contain perikarya and terminals of GHRH and SRIH neurons, and from exp lants of hypophysial stalk alone, which contain only terminals of GHRH and SRIH neurons. Clonidine failed to alter release of GHRH or SRIH from hypoth alamic slices, but stimulated release of GHRH from explants of hypophysial stalk. Blockade of SRIH receptors enabled clonidine to stimulate release of GHRH from slices of hypothalami, but also stimulated release of SRIH. Thes e results suggest that alpha (2)-adrenergic-induced secretion of GH occurs via a dual mechanism involving inhibition of SRIH neurons in the PeVN and d irect stimulation of GHRH release from axon terminals in the median eminenc e. Copyright (C) 2001 S. Karger AG, Basel.