Stress and the HPA Axis: Balancing Homeostasis and Fertility

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.

A neuroendocrine pathway modulating osmotic stress inDrosophila

“…whereas the two anterior pairs of Va neurons have axon terminations in the dorsal neural 14 sheath from which the peptides could be released into the hemolymph [53,54]. Thus, all 6…”

“…These hormones include Drosophila insulin-like peptides (DILPs), adipokinetic hormone (AKH), corazonin (Crz), leucokinin, diuretic hormone 44 (DH44) and capability gene-derived CAPA peptides [1][2][3][4][5][6][7][8][9][10][11][12]. In mammals, the hypothalamic-pituitary-adrenal (HPA) axis coordinates stress responses via the sequential secretion of corticotropinreleasing factor (CRF), adrenocorticotropic hormone (ACTH) and cortisol [13][14][15]. Although the insect pars intercerebralis-pars lateralis and corpora cardiaca are considered the functional equivalents of mammalian hypothalamus and pituitary gland, respectively [16], no explicit stress axis or stress hormones have yet been identified in insects.…”

Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71

“…6 In rats, early prenatal exposure to stressors such as multiple cage changes and exposure to fox odor induced an inflammatory state in the placenta, in which was associated with increased expression of pro-inflammatory cytokines and developmental disorders in the offspring. 9,10 The effects of glucocorticoids are mediated by the glucocorticoid receptor (GR), which translocates to the nucleus in a ligand-dependent manner and acts as a transcription factor to regulate gene expression. 8 Glucocorticoids are the primary mediators of the stress and immune response in the body.…”

“…Activation of the hypothalamicpituitary-adrenal (HPA) axis stimulates the production and release of glucocorticoids from the adrenal glands, which then act on tissues throughout the body to trigger physiological and behavioral changes that aid in coping with stress and the regulation of infection. 9,10 The effects of glucocorticoids are mediated by the glucocorticoid receptor (GR), which translocates to the nucleus in a ligand-dependent manner and acts as a transcription factor to regulate gene expression. 11 In late pregnancy, glucocorticoids are involved in the development and maturation of fetal organs.…”

Monosynaptic Input Mapping of Diencephalic Projections to the Cerebrospinal Fluid-Contacting Nucleus in the Rat

“…The CSF-contacting nucleus receives input from hypothalamic Pa, SO and DA and may participate in stress. Stress responses activate the hypothalamic-pituitary-adrenal (HPA) axis, where Pa can release hormones, such as the corticotropin-releasing hormone (CRH) and AVP, that affect biological activities (Joseph and Whirledge, 2017). The SO also expresses AVP as well as other substances, such as oxytocin, in response to a wide variety of stressors (Neumann, 2007;Borrow et al, 2018).…”