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Humans with loss of function mutations in<jats:italic><jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>3<\/jats:italic>or<jats:italic><jats:styled-content style=\"fixed-case\">TACR<\/jats:styled-content>3<\/jats:italic>, the genes encoding neurokinin B (<jats:styled-content style=\"fixed-case\">NKB<\/jats:styled-content>) or its receptor, neurokinin\u20103 receptor (<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>3R), respectively, present with severe congenital gonadotrophin deficiency and pubertal failure. Animal studies have shown ambiguous actions of<jats:styled-content style=\"fixed-case\">NKB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>3R signalling with respect to controlling puberty onset. The present study aimed to determine the role of endogenous<jats:styled-content style=\"fixed-case\">NKB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>3R signalling in the control of pulsatile luteinising hormone (<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content>) secretion and the timing of puberty onset, and also whether precocious pubertal onset as a result of an obesogenic diet is similarly regulated by this neuropeptide system. Prepubertal female rats, chronically implanted with i.c.v. cannulae, were administered<jats:styled-content style=\"fixed-case\">SB<\/jats:styled-content>222200, a<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>3R antagonist, or artificial cerebrospinal fluid via an osmotic mini\u2010pump for 14\u00a0days.<jats:styled-content style=\"fixed-case\">SB<\/jats:styled-content>222200 significantly delayed the onset of vaginal opening and first oestrus (as markers of puberty) compared to controls in both normal and high\u2010fat diet fed animals. Additionally, serial blood sampling, via chronic indwelling cardiac catheters, revealed that the increase in<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content>pulse frequency was delayed and that the<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content>pulse amplitude was reduced in response to<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>3R antagonism, regardless of dietary status. These data suggest that endogenous<jats:styled-content style=\"fixed-case\">NKB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>3R signalling plays a role in controlling the timing of puberty and the associated acceleration of gonadotrophin\u2010releasing hormone pulse generator frequency in the female rat.<\/jats:p>","DOI":"10.1111\/jne.12167","type":"journal-article","created":{"date-parts":[[2014,5,27]],"date-time":"2014-05-27T10:30:33Z","timestamp":1401186633000},"page":"521-527","source":"Crossref","is-referenced-by-count":22,"title":["Neurokinin B Receptor Antagonism Decreases Luteinising Hormone Pulse Frequency and Amplitude and Delays Puberty Onset in the Female Rat"],"prefix":"10.1111","volume":"26","author":[{"given":"S. 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