Document Detail


Expression of vesicular glutamate transporter-2 in gonadotrope and thyrotrope cells of the rat pituitary. Regulation by estrogen and thyroid hormone status.
MedLine Citation:
PMID:  16675529     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Immunocytochemical studies of the rat adenohypophysis identified a cell population that exhibits immunoreactivity for type-2 vesicular glutamate transporter (VGLUT2), a marker for glutamatergic neuronal phenotype. The in situ hybridization detection of VGLUT2 mRNA expression in adenohypophysial cells verified that VGLUT2 immunoreactivity is due to local synthesis of authentic VGLUT2. Dual-immunofluorescent studies of the hypophyses from male rats showed the presence of VGLUT2 in high percentages of LH (93.3 +/- 1.3%)-, FSH (44.7 +/- 3.9%)-, and TSH (70.0 +/- 5.6%)-immunoreactive cells and its much lower incidence in cells of the prolactin, GH, and ACTH phenotypes. Quantitative in situ hybridization studies have established that the administration of a single dose of 17-beta-estradiol (20 microg/kg; sc) to ovariectomized rats significantly elevated VGLUT2 mRNA in the adenohypophysis 16 h postinjection. Thyroid hormone dependence of VGLUT2 expression was addressed by the comparison of hybridization signals in animal models of hypo- and hyperthyroidism to those in euthyroid controls. Although hyperthyroidism had no effect on VGLUT2 mRNA, hypothyroidism increased adenohypophysial VGLUT2 mRNA levels. This coincided with a decreased ratio of VGLUT2-immunoreactive TSH cells, regarded as a sign of enhanced secretion. The presence of the glutamate marker VGLUT2 in gonadotrope and thyrotrope cells, and its up-regulation by estrogen or hypothyroidism, address the possibility that endocrine cells of the adenohypophysis may cosecrete glutamate with peptide hormones in an estrogen- and thyroid status-regulated manner. The exact roles of endogenous glutamate observed primarily in gonadotropes and thyrotropes, including its putative involvement in autocrine/paracrine regulatory mechanisms, will require clarification.
Authors:
Erik Hrabovszky; Imre Kalló; Gergely F Turi; Katalin May; Gábor Wittmann; Csaba Fekete; Zsolt Liposits
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-05-04
Journal Detail:
Title:  Endocrinology     Volume:  147     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-18     Completed Date:  2006-08-31     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3818-25     Citation Subset:  AIM; IM    
Affiliation:
Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, Budapest, 1083 Hungary. hrabovszky@koki.hu
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism
Estradiol / pharmacology*,  physiology
Female
Fluorescent Antibody Technique
Gene Expression / drug effects,  physiology
Glutamic Acid / metabolism*
Hyperthyroidism / metabolism,  physiopathology*
Hypothyroidism / metabolism,  physiopathology*
Immunoenzyme Techniques
Male
Pituitary Gland, Anterior / physiology*
RNA, Messenger / metabolism
Rats
Rats, Wistar
Thyroid Hormones / metabolism
Up-Regulation / drug effects,  physiology
Vesicular Glutamate Transport Protein 2 / genetics*,  metabolism
Chemical
Reg. No./Substance:
0/Biological Markers; 0/RNA, Messenger; 0/Slc17a6 protein, rat; 0/Thyroid Hormones; 0/Vesicular Glutamate Transport Protein 2; 50-28-2/Estradiol; 56-86-0/Glutamic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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