To investigate the role played by hypothalamic nonadrenaline (NE) in the regulation of TRH TSH 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 α methyl para tyrosine (α 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 third hr. The acute release of TSH evoked by cold exposure (CE) was prevented by pretreatment with α MpT 1 h before; when α 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 μg of clonidine hydrochloride in unstimulated rats caused a significant rise of basal TSH level 30, but not 10 min after the administration. Complete deafferentation of the medial basal hypothalamus (MBH), which destroys all the NE fibers afferent to this area, caused no change of thyrotropin secretion in basal conditions. Deafferented animals did not show any acute increase of TSH in response to CE. The results of this study provide evidence 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.
|Number of pages||7|
|Publication status||Published - 1977|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism