Abstract
An organism’s reproductive fitness is sensitive to the environment, integrating cues of resource availability, ecological factors, and hazards within its habitat. Events that challenge the environment of an organism activate the central stress response system, which is primarily mediated by the hypothalamic–pituitary–adrenal (HPA) axis. The regulatory functions of the HPA axis govern the cardiovascular and metabolic system, immune functions, behavior, and reproduction. Activation of the HPA axis by various stressors primarily inhibits reproductive function and is able to alter fetal development, imparting a biological record of stress experienced in utero. Clinical studies and experimental data indicate that stress signaling can mediate these effects through direct actions in the brain, gonads, and embryonic tissues. This review focuses on the mechanisms by which stress activation of the HPA axis impacts fertility and fetal development.
Highlights
Stress is commonly defined as a state of real or perceived threat to homeostasis that may challenge an organism’s well-being [1]
While basal glucocorticoid levels are necessary for fertility and fetal survival, upregulation due to acute HPA axis activation or exogenous treatment can have detrimental effects on fertility and fetal outcomes
The offspring of stressed mothers can present with abnormalities including reduced birth weight, higher levels of anxiety, higher levels of HPA axis function, and are at an increased risk of developing various physiological diseases
Summary
Stress is commonly defined as a state of real or perceived threat to homeostasis that may challenge an organism’s well-being [1]. The hypothalamic–pituitary–adrenal (HPA) axis, comprised of the hypothalamus, pituitary gland, and adrenal glands, regulates the body’s adaptive response to stress [1]. Activation of the HPA axis triggers neurons in the paraventricular nucleus (PVN) of the hypothalamus to release corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), which stimulate the anterior pituitary gland to produce and secrete adrenocorticotropic hormone (ACTH) [3]. Rising levels of cortisol inhibit further release of CRH and ACTH in a classic endocrine negative feedback loop, which enables the HPA axis to return to a physiological state following acute activation. As part of the physiological adaptation to stress, the HPA axis mediates the functions of the hypothalamic–adrenal–gonadal (HPG) axis, which is responsible for the maturation of the reproductive organs and the reproductive competence of an organism. The HPG axis controls the reproductive system through endocrine signaling, originating with hypothalamic secretion of gonadotropin-releasing hormone (GnRH). The purpose of this review is to briefly introduce the signaling mechanisms of stress hormones, summarize recent advances in our understanding of the effects of stress on fertility, and discuss current evidence that describes the long-term effects of stress experienced during in utero development
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