The role of corticotropin-releasing factor and interleukin-1 in the regulation of neurons controlling reproductive functions

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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.