{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T16:25:33Z","timestamp":1791044733537,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2017,7,2]],"date-time":"2017-07-02T00:00:00Z","timestamp":1498953600000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["15K18800"],"award-info":[{"award-number":["15K18800"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:p>Mammalian reproductive function is controlled by the hypothalamic\u2010pituitary\u2010gonadal (<jats:styled-content style=\"fixed-case\">HPG<\/jats:styled-content>) axis, which is suppressed under infectious stress conditions. By analysing the pulsatility of luteinising hormone (<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content>), we have previously demonstrated that prostaglandins (<jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content>s) in the central nervous system mediate infectious stress to suppress the activity of the <jats:styled-content style=\"fixed-case\">HPG<\/jats:styled-content> axis. The present study aimed to characterise the types of <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content>s responsible for suppression of the <jats:styled-content style=\"fixed-case\">HPG<\/jats:styled-content> axis. We focused on three major types of <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content>s: <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub>, <jats:styled-content style=\"fixed-case\">PGD<\/jats:styled-content><jats:sub>2<\/jats:sub> and <jats:styled-content style=\"fixed-case\">PGF<\/jats:styled-content><jats:sub>2\u03b1<\/jats:sub>. We used female rats overiectomised bilaterally 1\u00a0week before the experiments. Lipopolysaccharide (100\u00a0\u03bcg\u00a0kg<jats:sup>\u20131<\/jats:sup>) suppressed <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulses at the same time as enhancing the concentration of all three <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content>s in the cerebrospinal fluid, which was restored by indomethacin (10\u00a0mg\u00a0kg<jats:sup>\u20131<\/jats:sup>). Subsequently, we observed <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulsatility after a single injection of each <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content> and after co\u2010injection of <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub> with <jats:styled-content style=\"fixed-case\">PGF<\/jats:styled-content><jats:sub>2\u03b1<\/jats:sub> into the third cerebral ventricle. A single injection of <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub> dose\u2010dependently induced a transient increase in mean <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> concentration and <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulse amplitude, and <jats:styled-content style=\"fixed-case\">PGD<\/jats:styled-content><jats:sub>2<\/jats:sub> significantly increased the amplitude of <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulses, wereas <jats:styled-content style=\"fixed-case\">PGF<\/jats:styled-content><jats:sub>2\u03b1<\/jats:sub> did not affect <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulsatility. On the other hand, co\u2010injection of <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub> and <jats:styled-content style=\"fixed-case\">PGF<\/jats:styled-content><jats:sub>2\u03b1<\/jats:sub> induced a significant suppression of both the frequency and amplitude of <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulses. These results suggest that <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub> and <jats:styled-content style=\"fixed-case\">PGF<\/jats:styled-content><jats:sub>2\u03b1<\/jats:sub> can represent two of the mediators that suppress the <jats:styled-content style=\"fixed-case\">HPG<\/jats:styled-content> axis in situations of infectious stress. Moreover, the results imply that there are two contradictory effects of <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub> on <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> pulsatility: (i) enhancive when working alone and (ii) suppressive when working together with <jats:styled-content style=\"fixed-case\">PGF<\/jats:styled-content><jats:sub>2\u03b1<\/jats:sub>.<\/jats:p>","DOI":"10.1111\/jne.12490","type":"journal-article","created":{"date-parts":[[2017,5,23]],"date-time":"2017-05-23T20:11:45Z","timestamp":1495570305000},"source":"Crossref","is-referenced-by-count":4,"title":["Molecular species of prostaglandins involved in modulating luteinising hormone pulses of female rats under infectious stress conditions"],"prefix":"10.1111","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4842-6110","authenticated-orcid":false,"given":"T.","family":"Matsuwaki","sequence":"first","affiliation":[{"name":"Department of 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