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Stress and the Reproductive Axis

Authordc.contributor.authorToufexis, D. 
Authordc.contributor.authorRivarola, M. A. es_CL
Authordc.contributor.authorLara Peñaloza, Hernán es_CL
Authordc.contributor.authorViau, V. es_CL
Admission datedc.date.accessioned2014-12-30T13:26:03Z
Available datedc.date.available2014-12-30T13:26:03Z
Publication datedc.date.issued2014
Cita de ítemdc.identifier.citationJournal of Neuroendocrinology, 2014, 26, 573–586en_US
Identifierdc.identifier.otherdoi: 10.1111/jne.12179
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/121944
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractThere exists a reciprocal relationship between the hypothalamic-pituitary-adrenal (HPA) and the hypothalamic-pituitary-gonadal (HPG) axes, wherein the activation of one affects the function of the other and vice versa. For example, both testosterone and oestrogen modulate the response of the HPA axis, whereas activation of the stress axis, especially activation that is repeating or chronic, has an inhibitory effect upon oestrogen and testosterone secretion. Alterations in maternal care can produce significant effects on both HPG and HPA physiology, as well as behaviour in the offspring at adulthood. For example, changes in reproductive behaviour induced by altered maternal care may alter the expression of sex hormone receptors such as oestrogen receptor (ER)a that govern sexual behaviour, and may be particularly important in determining the sexual strategies utilised by females. Stress in adulthood continues to mediate HPG activity in females through activation of a sympathetic neural pathway originating in the hypothalamus and releasing norepinephrine into the ovary, which produces a noncyclic anovulatory ovary that develops cysts. In the opposite direction, sex differences and sex steroid hormones regulate the HPA axis. For example, although serotonin (5-HT) has a stimulatory effect on the HPA axis in humans and rodents that is mediated by the 5-HT1A receptor, only male rodents respond to 5-HT1A antagonism to show increased corticosterone responses to stress. Furthermore, oestrogen appears to decrease 5-HT1A receptor function at presynaptic sites, yet increases 5-HT1A receptor expression at postsynaptic sites. These mechanisms could explain the heightened stress HPA axis responses in females compared to males. Studies on female rhesus macaques show that chronic stress in socially subordinate female monkeys produces a distinct behavioural phenotype that is largely unaffected by oestrogen, a hyporesponsive HPA axis that is hypersensitive to the modulating effects of oestrogen, and changes in 5-HT1A receptor binding in the hippocampus and hypothalamus of social subordinate female monkeys that are restored or inverted by oestrogen replacement. This review summarises all of these studies, emphasising the profound effect that the interaction of the reproductive and stress axes may have on human reproductive health and emotional wellbeing.en_US
Patrocinadordc.description.sponsorshipThis work was funded by Fondecyt 1130049 (HL), CONICET and SECyT-UNC (MAR) NIH grants: HD 046501 (MW), MH081816 (DT), F31MH085445 (VM) and RR00165, and the Canadian Institutes of Health Research CIHR MOP- 42555 (VV).en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherBritish Society for Neuroendocrinologyen_US
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Keywordsdc.subjectreproductionen_US
Títulodc.titleStress and the Reproductive Axisen_US
Document typedc.typeArtículo de revistaen_US


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Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile