The Role of Central Noradrenergic Neurons in the Control of Thyrotropin Secretion in the Rat

Publisher Website
Google Scholar
Abstract
To investigate the role played by hypothalamic noradrenaline (NE) in the regulation of TRH-TSH [thyrotropin-releasing hormone-thyrotropin] release during tonic and cold activated conditions, drugs and surgical procedures able to interfere with central NE tonus were utilized. The time course of the effect of .alpha.-methyl-p-tyrosine (.alpha.-MpT) on basal TSH secretion was followed. The tyrosine hydroxylase (TH) inhibitor was unable to modify TSH plasma levels, whereas NE hypothalamic content decreased beginning with the 3rd h. Acute release of TSH evoked by cold exposure (CE) was prevented by pretreatment with .alpha.-MpT 1 h before; when .alpha.-MpT was followed 40 min later by clonidine, a central noradrenergic stimulating agent, TSH response to cold, previously blocked by the TH inhibitor was restored. Intraventricular injection of 10 .mu.g of clonidine hydrochloride in unstimulated rats significantly raised of basal TSH levels 30, but not 10 min after administration. Complete deafferentation of the medial basal hypothalamus (MBH), which destroys all the NE fibers afferent to this area, caused no change of TSH secretion in basal conditions. Deafferented animals did not show any acute increase of TSH in response to CE. Evidence was provided that NE may be the catecholamine (CA) mediating the rise in TSH following CE and that the direct stimulation of central NE receptors can evoke a massive TSH release from the anterior pituitary gland also in basal conditions.