Noradrenaline stimulates somatostatin release from incubated slices of the amygdala and the hypothalamic preoptic area

Abstract

Neurotransmitter effects were studied on in vitro release of immunoreactive somatostatin (SRIF) from slices prepared from several regions of the rat brain: mediobasal hypothalamus (MBH), preoptic anterior hypothalamic area (POA) and amygdaloid complex (AMY). Potassium (K +, 56 mM) stimulated SRIF release in all structures tested in a calcium dependent manner. Morphine, dopamine, GABA and serotonin did not modify SRIF release in any structure; noradrenaline (NA) was not effective on MBH slices, but elicited a dose-dependent stimulation of SRIF release from POA and AMY (ED 50 = 6.4nMand3.6 ±nM respectively). Conveerse orders of potency of adrenergic agonist were observed in both structures (POA, adrenalin > noradrenaline > isoproterenol; AMY, isopreterenol > adrenaline > noradrenaline). Phentolamine blocked NA-induced SRIF release in the POA while propanolol was ineffective. On the contrary, propanolol, but not phentolamine, antagonized NA stimulation in the amygdala. The data suggest that NA acting through specific receptors modulate SRIF release from POA and AMY. In POA, NA effect seems mediated through α adrenergic receptors while in AMY, β receptors are involved. The possibility that these interactions of NA with SRIF release are correlated with effects of NA on growth hormone secretion or on epileptic events is discussed.