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Roles For Androgens In Mediating The Sex Differences Of Neuroendocrine And Behavioral Stress Responses

In addition, contingent (i.e. self) administration of drugs can reduce HPA and ANS responses169,176, 180, 181. Importantly, acute experiences with naturally rewarding stimuli do not always evoke stress-like responses182–185,186, 187. Genomic actions occur following binding to glucocorticoid receptor and, in the case of some tissues, mineralocorticoid receptors , which act as ligand-activated transcription factors to affect broad, long-latency and biologically long-acting changes in gene transcription62. The MR has a high affinity for endogenous glucocorticoids and is extensively bound even during the circadian nadir of corticosteroid secretion. The GR has a lower affinity and is extensively bound only at relatively high levels of corticosteroids, such as during stress responses121.

143.Kinsella MT, Monk C. Impact of maternal stress, depression and anxiety on fetal neurobehavioral development. 41.Cota D, Steiner MA, Marsicano G, Cervino C, Herman JP, Grubler Y, Stalla J, Pasquali R, Lutz B, Stalla GK, Pagotto U. Requirement of cannabinoid receptor type 1 for the basal modulation of hypothalamic-pituitary-adrenal axis function. 39.Korbonits M, Kaltsas G, Perry LA, Putignano P, Grossman AB, Besser GM, Trainer PJ. The growth hormone secretagogue hexarelin stimulates the hypothalamo-pituitary-adrenal axis via arginine vasopressin. 29.Wong ML, Licinio J, Pasternak KI, Gold PW. Localization of corticotropin-releasing hormone receptor mRNA in adult rat brain by in situ hybridization histochemistry. 8.Kiss A, Aguilera G. Participation of alpha 1-adrenergic receptors in the secretion of hypothalamic corticotropin-releasing hormone during stress.

Stress-induced activation of the dorsal part of medial parvocellular paraventricular nucleus of the hypothalamus originates in several brain regions (excitatory inputs colored blue with solid lines and inhibitory inputs colored red with dashed lines). The paraventricular nucleus of the hypothalamus receives direct noradrenergic, adrenergic and peptidergic innervation from the nucleus of the solitary tract . The dorsomedial component of dorsomedial hypothalamus and arcuate nucleus provide intrahypothalamic stress excitation.

Hyperkalaemia can also follow major physical injury causing disruption of cell membranes , leading to the release of large amounts of intracellular potassium that have accumulated via the Na+ K+ pump . Aldosterone promotes the human environment interaction in california reabsorption of Na+ in the kidney, thereby increasing plasma Na+ concentration . This encourages the movement of water from the tissues into the blood vessels by osmosis, thereby increasing blood volume and blood pressure.

The anterior part of the bed nucleus of the stria terminalis , particularly the anteroventral nucleus of the BST , activates HPA axis stress responses. The PVN also receives stress-excitatory drive from the avBST, dorsal raphe, tuberomammillary nucleus, supramammillary nucleus, and spinal cord, among others . Activation of the PVNmpd is inhibited by numerous hypothalamic circuits, including the medial preoptic area , ventrolateral component of dorsomedial hypothalamus and local neurons in the peri-PVN region , encompassing the PVN surround and the subparaventricular zone. The posterior subregions of the bed nucleus of the stria terminalis provides a prominent forebrain inhibition of HPA axis responses; the majority of these inputs are GABAergic. The brainstem is able to generate rapid hypothalamus-pituitary-adrenal axis and autonomic nervous system responses via direct projections to hypophysiotrophic neurons in the paraventricular nucleus of the hypothalamus or to preganglionic autonomic neurons (bottom-up regulation). In contrast, forebrain limbic regions have no direct connections with the HPA axis or the ANS and thus require intervening synapses prior to accessing autonomic or neuroendocrine neurons (top-down regulation).

Interestingly, there are CRH peptidergic neurons in the amygdala which respond positively to glucocorticoids and whose activation leads to stress system stimulation and anxiety. Of note, CRH neurons in the central nucleus of the amygdala send projections to the PVN parvocellular regions and the parabrachial nucleus of the brain stem which are considered crucial for CRH-induced neuroendocrine, autonomic and behavioral effects. Moreover, CRH fibers also interconnect the amygdala with the bed nucleus of the stria terminalis and the hypothalamus . Conversely to the stimulatory CRH and norepinephrine effect, the hippocampus exerts a tonic and stimulated inhibitory effect on the amygdala activity and the PVN CRH and LC/NE-sympathetic systems. Indeed, the hippocampus plays an important role in shutting off the HPA stress response; hence, hippocampal atrophy or damage impairs this shut off function and can lead to prolonged HPA responses to psychological stressors . Accordingly, Lupien et al. have shown that progressively increased salivary cortisol levels during annual exams over a 5-year period can predict reduced hippocampal volume and decreased performance on hippocampal-dependent learning and memory tasks .

Furthermore, dysregulation of these systems can underlie the sex biases in risk for complex, stress-related diseases that are found in humans. Although many studies have explored the role of estrogen and estrogen receptors in mediating sex differences in stress-related behaviors and HPA function, much less consideration has been given to the role of androgens. While circulating androgens can act by binding and activating androgen receptors, they can also act by metabolism to estrogenic molecules to impact estrogen signaling in the brain and periphery.