{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T16:25:38Z","timestamp":1791044738784,"version":"4.1.0"},"reference-count":92,"publisher":"The Endocrine Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,7,1]]},"abstract":"<jats:p>Acute systemic stress disrupts reproductive function by inhibiting pulsatile gonadotropin secretion. The underlying mechanism involves stress-induced suppression of the GnRH pulse generator, the functional unit of which is considered to be the hypothalamic arcuate nucleus kisspeptin\/neurokinin B\/dynorphin A neurons. Agonists of the neurokinin B (NKB) receptor (NK3R) have been shown to suppress the GnRH pulse generator, in a dynorphin A (Dyn)-dependent fashion, under hypoestrogenic conditions, and Dyn has been well documented to mediate several stress-related central regulatory functions. We hypothesized that the NKB\/Dyn signaling cascade is required for stress-induced suppression of the GnRH pulse generator. To investigate this ovariectomized rats, iv administered with Escherichia coli lipopolysaccharide (LPS) following intracerebroventricular pretreatment with NK3R or \u03ba-opioid receptor (Dyn receptor) antagonists, were subjected to frequent blood sampling for hormone analysis. Antagonism of NK3R, but not \u03ba-opioid receptor, blocked the suppressive effect of LPS challenge on LH pulse frequency. Neither antagonist affected LPS-induced corticosterone secretion. Hypothalamic arcuate nucleus NKB neurons project to the paraventricular nucleus, the major hypothalamic source of the stress-related neuropeptides CRH and arginine vasopressin (AVP), which have been implicated in the stress-induced suppression of the hypothalamic-pituitary-gonadal axis. A separate group of ovariectomized rats was, therefore, used to address the potential involvement of central CRH and\/or AVP signaling in the suppression of LH pulsatility induced by intracerebroventricular administration of a selective NK3R agonist, senktide. Neither AVP nor CRH receptor antagonists affected the senktide-induced suppression of the LH pulse; however, antagonism of type 2 CRH receptors attenuated the accompanying elevation of corticosterone levels. These data indicate that the suppression of the GnRH pulse generator by acute systemic stress requires hypothalamic NKB\/NK3R signaling and that any involvement of CRH therewith is functionally upstream of NKB.<\/jats:p>","DOI":"10.1210\/en.2013-2038","type":"journal-article","created":{"date-parts":[[2014,4,7]],"date-time":"2014-04-07T15:44:08Z","timestamp":1396885448000},"page":"2589-2601","source":"Crossref","is-referenced-by-count":32,"title":["Neurokinin B Signaling in the Female Rat: a Novel Link Between Stress and Reproduction"],"prefix":"10.1210","volume":"155","author":[{"given":"P.","family":"Grachev","sequence":"first","affiliation":[{"name":"Division of Women\u2019s Health (P.G., X.F.L., M.H.H., S.Y.L., K.T.O.), School of Medicine, King\u2019s College London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"X.F.","family":"Li","sequence":"first","affiliation":[{"name":"Division of Women\u2019s Health (P.G., X.F.L., M.H.H., S.Y.L., K.T.O.), 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