Endocrinology, Vol 100, 738-744, Copyright © 1977 by Endocrine Society
The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat
L Annunziato, G Di Renzo, G Lombardi, F Scopacasa, G Schettini, P Preziosi and U Scapagnini
Department of Pharmacology and Endocrinology, IInd Faculty of Medicine, University of Naples, Italy.
To investigate the role played by hypothalamic noradrenaline (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 alpha- methyl-para-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 third hour. The 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 micrograms of clonidine hydrochloride in unstimulated rats
caused a significant rise of basal TSH levels 3, but not 10 min after the
administration. Complex 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.
