Document Detail


Estrogen regulation of neurotrophin expression in sympathetic neurons and vascular targets.
MedLine Citation:
PMID:  17289002     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We hypothesize that estrogen exerts a modulatory effect on sympathetic neurons to reduce neural cardiovascular tone and that these effects are modulated by nerve growth factor (NGF), a neurotrophin that regulates sympathetic neuron survival and maintenance. We examined the effects of estrogen on NGF and tyrosine hydroxylase (TH) protein content in specific vascular targets. Ovariectomized, adult Sprague-Dawley rats were implanted with placebo or 17beta-estradiol (release rate, 0.05 mg/day). Fourteen days later, NGF levels in the superior cervical ganglia (SCG) and its targets, the heart, external carotid artery, and the extracerebral blood vessels, as well as estrogen receptor alpha (ERalpha) content levels in the heart, were determined using semi-quantitative Western blot analysis. TH levels in the SCG and extracerebral blood vessels were determined by Western blotting and immunocytochemistry, respectively. Circulating levels of 17beta-estradiol and prolactin (PRL) were quantified by RIA. Estrogen replacement significantly decreased NGF protein in the SCG and its targets, the external carotid artery, heart and extracerebral blood vessels. TH protein associated with the extracerebral blood vessels was also significantly decreased, but ERalpha levels were significantly increased in the heart following estrogen replacement. These results indicate that estrogen reduces NGF protein content in sympathetic vascular targets, which may lead to decreased sympathetic innervations to these targets, and therefore reduced sympathetic regulation. In addition, the estrogen-induced increase in ERalpha levels in the heart, a target tissue of the SCG, suggests that estrogen may sensitize the heart to further estrogen modulation, and possibly increase vasodilation of the coronary vasculature.
Authors:
Gurjinder Kaur; James Janik; Lori G Isaacson; Phyllis Callahan
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-01-08
Journal Detail:
Title:  Brain research     Volume:  1139     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-05     Completed Date:  2007-05-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  6-14     Citation Subset:  IM    
Affiliation:
Center for Neuroscience and Behavior, Department of Zoology, Miami University, Oxford, OH 45056, USA. gkaur@nki.rfmh.org
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MeSH Terms
Descriptor/Qualifier:
Adrenergic Fibers / metabolism
Animals
Brain / blood supply
Carotid Artery, External / innervation,  metabolism
Cerebral Arteries / innervation,  metabolism
Down-Regulation
Estradiol / physiology*
Estrogen Receptor alpha / metabolism
Estrogen Replacement Therapy
Female
Heart / innervation
Immunohistochemistry
Myocardium / metabolism
Nerve Growth Factor / metabolism*
Neurons / metabolism*
Ovariectomy
Prolactin / blood
Protein Isoforms
Rats
Rats, Sprague-Dawley
Superior Cervical Ganglion / cytology,  metabolism*
Tyrosine 3-Monooxygenase / metabolism*
Vasodilation / physiology
Chemical
Reg. No./Substance:
0/Estrogen Receptor alpha; 0/Protein Isoforms; 50-28-2/Estradiol; 9002-62-4/Prolactin; 9061-61-4/Nerve Growth Factor; EC 1.14.16.2/Tyrosine 3-Monooxygenase

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


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