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The Molecular Endocrinology Laboratory, CHUL Research Center, Centre Hospitalier de I'Universite Laval, Quebec (PQ) Canada, G1V 4G2
The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute 10010 North Torrey Pines Road, La Jolla, California 9203
Correspondence: Address requests for reprints to: Serge Rivest, Ph.D., Molecular Endocrinology Laboratory, CHUL Research Center, Centre Hospitalier de l'Université Laval, 2705, Boulevard Laurier, Quebec (P.Q.), Canada, G1V 4G2.
Abstract
I. Introduction: DISRUPTION of reproductive functions in mammals is a well known consequence of stress. The changes undergone by the hypothalamic-pituitary-gonadal (HPG)1 axis are influenced by the type of stimulus, its duration, the gender of the experimental animals used, and the species studied. To understand how stress inhibits fertility, we must first define "stress." Although this concept has been widely and eloquently discussed (1), we have found it useful to define stress as any threat, real or perceived, that compromises homeostasis. All noxious signals, however, are not equal. When considering the potential effect exerted by a noxious stimulus on the pituitary function, one realizes that, although many so-called stressors can alter the release of ACTH and PRL, usually only intense and/or prolonged signals will interfere with gonadotropin secretion. This suggests first that the responses of the hypothalamic-pituitary-adrenal (HPA) and HPG axes can be dissociated during exposure to a stress (discussed below) and second, that each description of the response of the HPG axis to noxious stimuli must be accompanied by the precise characterization of these stimuli.
Footnotes
* Supported by the Foundation for Research, Inc., and the Fonds de la recherche en santé du Quebec (FRSQ), the Canadian Medical Research Council, the Natural Sciences and Engineering Research Council of Canada, and NIH Grants HD-13527 and DK-26741.
Scholar of the Canadian Medical Research Council.
Foundation for Research Investigator.
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