The Aryl Hydrocarbon Receptor Pathway and Sexual Differentiation of Neuroendocrine Functions

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 d...

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Bibliographic Details
Published in:	Endocrinology (Philadelphia) Vol. 147; no. 6; pp. s33 - s42
Main Authors:	Petersen, Sandra L, Krishnan, Sudha, Hudgens, Edward D
Format:	Journal Article Conference Proceeding
Language:	English
Published:	Bethesda, MD Endocrine Society 01-06-2006 Oxford University Press
Subjects:	Animal models Animals Aromatic compounds Biological and medical sciences Carcinogens Contaminants Dioxins Dioxins - toxicity Environmental effects Environmental Exposure Estradiol - physiology Female Fundamental and applied biological sciences. Psychology gamma-Aminobutyric Acid - physiology Glutamic Acid - physiology Humans Hydrocarbons Ligands Neuroendocrine system Neurons - drug effects Neurosecretory Systems - drug effects Neurosecretory Systems - embryology Ovulation Perinatal exposure Polychlorinated Dibenzodioxins - toxicity Pregnancy Prenatal Exposure Delayed Effects Receptors Receptors, Aryl Hydrocarbon - physiology Reproduction - drug effects Sex Differentiation Vertebrates: endocrinology γ-Aminobutyric acid Ah receptor Sexual differentiation
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Summary:	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.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1
ISSN:	0013-7227 1945-7170
DOI:	10.1210/en.2005-1157