Rhythmic expression of clock genes in the ependymal cell layer of the third ventricle of rodents is independent of melatonin signaling

Shinobu Yasuo, Charlotte Von Gall, David R. Weaver, Horst Werner Korf

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Reproductive physiology is regulated by the photoperiod in many mammals. Decoding of the photoperiod involves circadian clock mechanisms, although the molecular basis remains unclear. Recent studies have shown that the ependymal cell layer lining the infundibular recess of the third ventricle (EC) is a key structure for the photoperiodic gonadal response. The EC exhibits daylength-dependent changes in the expression of photoperiodic output genes, including the type 2 deiodinase gene (Dio2). Here we investigated whether clock genes (Per1 and Bmal1) and the albumin D-binding protein gene (Dbp) are expressed in the EC of Syrian hamsters, and whether their expression differs under long-day and short-day conditions. Expression of all three genes followed a diurnal rhythm; expression of Per1 and Dbp in the EC peaked around lights-off, and expression of Bmal1 peaked in the early light phase. The amplitude of Per1 and Dbp expression was higher in hamsters kept under long-day conditions than in those kept under short-day conditions. Notably, the expression of these genes was not modified by exogenous melatonin within 25 h after injection, whereas Dio2 expression was inhibited 19 h after injection. Targeted melatonin receptor (MT1, MT2, and both MT1 and MT2) disruption in melatonin-proficient C3H mice did not affect the rhythmic expression of Per1 in the EC. These data show the existence of a molecular clock in the rodent EC. In the hamster, this clock responds to long-term changes in the photoperiod, but is independent of acute melatonin signals. In mice, the EC clock is not affected by deletion of melatonin receptors.

Original languageEnglish
Pages (from-to)2443-2450
Number of pages8
JournalEuropean Journal of Neuroscience
Volume28
Issue number12
DOIs
Publication statusPublished - Dec 1 2008
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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