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Vertebrate reproductive science and technology
RESEARCH ARTICLE

Ontogeny of clock and KiSS-1 metastasis-suppressor (Kiss1) gene expression in the prepubertal mouse hypothalamus

Cassandra C. Yap A , Peter J. Mark A , Brendan J. Waddell A and Jeremy T. Smith A B
+ Author Affiliations
- Author Affiliations

A School of Anatomy, Physiology and Human Biology, The University of Western Australia, Perth, WA 6009, Australia.

B Corresponding author. Email: jeremy.smith@uwa.edu.au

Reproduction, Fertility and Development 29(10) 1971-1981 https://doi.org/10.1071/RD16198
Submitted: 12 May 2016  Accepted: 23 November 2016   Published: 21 December 2016

Abstract

Kisspeptin is crucial for the generation of the circadian-gated preovulatory gonadotrophin-releasing hormone (GnRH)–LH surge in female rodents, with expression in the anteroventral periventricular nucleus (AVPV) peaking in the late afternoon of pro-oestrus. Given kisspeptin expression is established before puberty, the aim of the present study was to investigate kisspeptin and clock gene rhythms during the neonatal period. Anterior and posterior hypothalami were collected from C57BL/6J mice on Postnatal Days (P) 5, 15 and 25, at six time points across 24 h, for analysis of gene expression by reverse transcription–quantitative polymerase chain reaction. Expression of aryl hydrocarbon receptor nuclear translocator-like gene (Bmal1) and nuclear receptor subfamily 1, group D, member 2 (Rev-erbα) in the anterior hypothalamus (containing the suprachiasmatic nucleus) was not rhythmic at P5 or P15, but Bmal1 expression exhibited rhythmicity in P25 females, whereas Rev-erbα expression was rhythmic in P25 males. KiSS-1 metastasis-suppressor (Kiss1) expression did not exhibit time-of-day variation in the anterior (containing the AVPV) or posterior (containing the arcuate nucleus) hypothalami in female and male mice at P5, P15 or P25. The data indicate that the kisspeptin circadian peak in expression observed in the AVPV of pro-oestrous females does not manifest at P5, P15 or P25, likely due to inadequate oestrogenic stimuli, as well as incomplete development of clock gene rhythmicity before puberty.

Additional keywords: neonate, neuroendocrinology, neuropeptide, puberty, reproduction.


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