{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T09:02:29Z","timestamp":1790586149617,"version":"4.1.0"},"reference-count":62,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2014,11,17]],"date-time":"2014-11-17T00:00:00Z","timestamp":1416182400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001505","name":"New Zealand Health Research Council","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2014,12]]},"abstract":"<jats:p>\n                    Hyperprolactinaemia is a major cause of infertility in both males and females, although the mechanism by which prolactin inhibits the reproductive axis is not clear. The aim of the present study was to test the hypothesis that elevated prolactin causes suppression of kisspeptin expression in the hypothalamus, resulting in reduced release of gonadotrophin\u2010releasing hormone (GnRH) and consequent infertility. In oestrogen\u2010treated ovariectomised  mice, chronic prolactin\u2010treatment prevented the rise in luteinising hormone (\n                    <jats:styled-content style=\"fixed-case\">LH)<\/jats:styled-content>\n                    seen in vehicle\u2010treated mice.\n                    <jats:italic>Kiss1<\/jats:italic>\n                    m\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    was significantly suppressed in both the rostral periventricular region of the third ventricle (\n                    <jats:styled-content style=\"fixed-case\">RP<\/jats:styled-content>\n                    3\n                    <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\n                    ) and arcuate nucleus after prolactin treatment. Exogenous prolactin treatment induced phosphorylated signal transducer and activator of transcription 5 (pSTAT5) in kisspeptin neurones, and suppression of endogenous prolactin using bromocriptine reduced levels of p\n                    <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>\n                    5 in kisspeptin neurones, suggesting that prolactin acts directly on kisspeptin neurones. By contrast, fewer than 1% of\n                    <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>\n                    n\n                    <jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>\n                    neurones expressed p\n                    <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>\n                    5 in either dioestrous or lactating mice. As reported previously, there was significant suppression of kisspeptin m\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    and protein in the\n                    <jats:styled-content style=\"fixed-case\">RP<\/jats:styled-content>\n                    3\n                    <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\n                    on day 7 of lactation, although not in the arcuate nucleus. Bromocriptine treatment significantly increased\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>\n                      iss1\n                    <\/jats:italic>\n                    m\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    expression in the\n                    <jats:styled-content style=\"fixed-case\">RP<\/jats:styled-content>\n                    3\n                    <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\n                    , although not to dioestrous levels. Unilateral thelectomy, aiming to eliminate sensory inputs from nipples on one side of the body, failed to alter the reduction in the number of kisspeptin neurones observed in the\n                    <jats:styled-content style=\"fixed-case\">RP<\/jats:styled-content>\n                    3\n                    <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\n                    . These data demonstrate that chronic prolactin administration suppressed serum\n                    <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content>\n                    , and reduced\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>\n                      iss1\n                    <\/jats:italic>\n                    m\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    levels in both the\n                    <jats:styled-content style=\"fixed-case\">RP<\/jats:styled-content>\n                    3\n                    <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">arcuate nucleus<\/jats:styled-content>\n                    , consistent with the hypothesis that prolactin\u2010induced suppression of kisspeptin secretion might mediate the inhibitory effects of prolactin on\n                    <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>\n                    n\n                    <jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>\n                    secretion. During lactation, however, the suppression of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>\n                      iss1\n                    <\/jats:italic>\n                    m\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    in the\n                    <jats:styled-content style=\"fixed-case\">RP<\/jats:styled-content>\n                    3\n                    <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\n                    was only partially reversed by the administration of bromocriptine to block elevated levels of prolactin, suggesting that, although elevated prolactin contributes to lactational anovulation, additional non\u2010neural factors must also contribute to the lactation\u2010induced suppression of kisspeptin neurones.\n                  <\/jats:p>","DOI":"10.1111\/jne.12223","type":"journal-article","created":{"date-parts":[[2014,9,10]],"date-time":"2014-09-10T08:07:05Z","timestamp":1410336425000},"page":"898-908","source":"Crossref","is-referenced-by-count":91,"title":["Prolactin Regulation of Kisspeptin Neurones in the Mouse Brain and its Role in the Lactation\u2010Induced Suppression of Kisspeptin Expression"],"prefix":"10.1111","volume":"26","author":[{"given":"R. S. E.","family":"Brown","sequence":"first","affiliation":[{"name":"Department of Anatomy Centre for Neuroendocrinology School of Medical Sciences University of Otago Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. E.","family":"Herbison","sequence":"additional","affiliation":[{"name":"Department of Physiology Centre for Neuroendocrinology School of Medical Sciences University of Otago Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. R.","family":"Grattan","sequence":"additional","affiliation":[{"name":"Department of Anatomy Centre for Neuroendocrinology School of Medical Sciences University of Otago Dunedin New 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