help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Endocrinology, doi:10.1210/en.2005-1157
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Petersen, S. L.
Right arrow Articles by Hudgens, E. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Petersen, S. L.
Right arrow Articles by Hudgens, E. D.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN
*ESTRADIOL
*GLUTAMIC ACID HYDROCHLORIDE
Endocrinology Vol. 147, No. 6 s33-s42
Copyright © 2006 by The Endocrine Society


Supplement

The Aryl Hydrocarbon Receptor Pathway and Sexual Differentiation of Neuroendocrine Functions

Sandra L. Petersen, Sudha Krishnan and Edward D. Hudgens

Department of Biology, Molecular and Cellular Biology Graduate Program, University of Massachusetts—Amherst, Amherst, Massachusetts 01003

Address all correspondence and requests for reprints to: Sandra L. Petersen, 611 North Pleasant Street, Department of Biology, University of Massachusetts–Amherst, Amherst, Massachusetts 01003. E-mail: sandyp{at}bio.umass.edu.

Abstract

Historically, much of the research on health effects of environmental pollutants focused on ascertaining whether compounds were carcinogenic. More recent findings show that environmental contaminants also exert insidious effects by disrupting hormone action. Of particular concern are findings that developmental exposure to dioxins, chemicals that act through the aryl hydrocarbon receptor pathway, permanently alters sexually differentiated neural functions in animal models. In this review, we focus on mechanisms through which dioxins disrupt neuroendocrine development as exemplified by effects on a brain region critical for ovulation in rodents. We also provide evidence that dysregulation of GABAergic neural development may be a general mechanism underlying a broad spectrum of effects seen after perinatal dioxin exposure.




This article has been cited by other articles:


Home page
J EndocrinolHome page
W. Xia, D. D Mruk, W. M Lee, and C Y. Cheng
Unraveling the molecular targets pertinent to junction restructuring events during spermatogenesis using the Adjudin-induced germ cell depletion model
J. Endocrinol., March 1, 2007; 192(3): 563 - 583.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2006 by The Endocrine Society