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, U. Scapagnini

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)738-744
Number of pages7
JournalEndocrinology
Volume100
Issue number3
Publication statusPublished - 1977

Fingerprint

Adrenergic Neurons
Thyrotropin
Tyrosine
Tyrosine 3-Monooxygenase
Clonidine
Intraventricular Injections
Middle Hypothalamus
Anterior Pituitary Gland
Catecholamines
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Annunziato, L., Di Renzo, G., Lombardi, G., Scopacasa, F., Schettini, G., Preziosi, P., & Scapagnini, U. (1977). The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat. Endocrinology, 100(3), 738-744.

The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat. / Annunziato, L.; Di Renzo, G.; Lombardi, G.; Scopacasa, F.; Schettini, G.; Preziosi, P.; Scapagnini, U.

In: Endocrinology, Vol. 100, No. 3, 1977, p. 738-744.

Research output: Contribution to journalArticle

Annunziato, L, Di Renzo, G, Lombardi, G, Scopacasa, F, Schettini, G, Preziosi, P & Scapagnini, U 1977, 'The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat', Endocrinology, vol. 100, no. 3, pp. 738-744.
Annunziato L, Di Renzo G, Lombardi G, Scopacasa F, Schettini G, Preziosi P et al. The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat. Endocrinology. 1977;100(3):738-744.
Annunziato, L. ; Di Renzo, G. ; Lombardi, G. ; Scopacasa, F. ; Schettini, G. ; Preziosi, P. ; Scapagnini, U. / The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat. In: Endocrinology. 1977 ; Vol. 100, No. 3. pp. 738-744.
@article{83ee58e2b58041e5a9af2f42b7b61eff,
title = "The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat",
abstract = "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.",
author = "L. Annunziato and {Di Renzo}, G. and G. Lombardi and F. Scopacasa and G. Schettini and P. Preziosi and U. Scapagnini",
year = "1977",
language = "English",
volume = "100",
pages = "738--744",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The Endocrine Society",
number = "3",

}

TY - JOUR

T1 - The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat

AU - Annunziato, L.

AU - Di Renzo, G.

AU - Lombardi, G.

AU - Scopacasa, F.

AU - Schettini, G.

AU - Preziosi, P.

AU - Scapagnini, U.

PY - 1977

Y1 - 1977

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0017348186&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0017348186&partnerID=8YFLogxK

M3 - Article

C2 - 401025

AN - SCOPUS:0017348186

VL - 100

SP - 738

EP - 744

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 3

ER -