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Mol Cell Endocrinol. 2014 Mar 25;385(1-2):71-7. doi: 10.1016/j.mce.2013.08.014. Epub 2013 Sep 4.

Influence of stress-induced intermediates on gonadotropin gene expression in gonadotrope cells.

Author information

1
Department of Reproductive Medicine and Center for Reproductive Science and Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0674, United States. Electronic address: kbchurch@ucsd.edu.
2
Department of Reproductive Medicine and Center for Reproductive Science and Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0674, United States.

Abstract

Despite extensive investigation, a comprehensive understanding of the mechanisms whereby stress impacts fertility remains elusive. Since the 1930s, when Hans Selye popularized studying adaptations to stress (Selye, 1937), we have learned that compensatory mechanisms involve a complex interplay of neural and hormonal processes that allow various body functions to adjust to stress, in a coordinated manner. In terms of reproduction, the adjustment to a stressor interferes with integrated functioning at multiple levels of regulation--the hypothalamus, anterior pituitary gland, gonads, and neural centers coordinating behavior. Various mediators are postulated to participate in reproductive suppression. These include catecholamines, cytokines, prostaglandins, endogenous opioid peptides, and hormones of the hypothalamic-pituitary-adrenal axis. This review focuses on one class of mediators, the glucocorticoids, and provides our views on the relevance and mode of action of this inhibitory intermediate within the anterior pituitary gonadotrope, as a potential cellular site whereby glucocorticoids contribute to stress-induced reproductive suppression.

KEYWORDS:

Follicle-stimulating hormone; Glucocorticoids; Gonadotropin-releasing hormone; Luteinizing hormone; Pituitary

PMID:
24012628
PMCID:
PMC3942370
DOI:
10.1016/j.mce.2013.08.014
[Indexed for MEDLINE]
Free PMC Article

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