Photoperiodic control of TSH-β expression in the mammalian pars tuberalis has different impacts on the induction and suppression of the hypothalamo-hypopysial gonadal axis

S. Yasuo, T. Yoshimura, S. Ebihara, H. W. Korf

Research output: Contribution to journalArticlepeer-review

47 Citations (Scopus)

Abstract

Seasonal reproduction depends on photoperiod-regulated activation or suppression of the gonadal axis. Recent studies in quail have identified long-day induced . TSH-β expression in the pars tuberalis (PT) as a rapid trigger of gonadal activation. Thyroid-stimulating hormone (TSH) induces type 2 deiodinase (. Dio2) in the ependymal cell layer (EC) of the infundibular recess to stimulate the gonadal axis. A similar mechanism is proposed in sheep and mice, but the experimental data on the temporal patterns of induction and suppression of . TSH-β and . Dio2 expression are incomplete. In the present study, we examined the expression of . TSH-β and . Dio2 in hamsters transferred from short- to long-day conditions for 9 days, and demonstrate the induction of . TSH-β and . Dio2 on day 8 after transition. These data demonstrate the close relationship between . TSH-β and . Dio2 expression in the inductive pathway. The temporal expression of . TSH-β and . Dio2 in the suppressive pathway was also examined by s.c. melatonin injection, which mimics the transition from long to short days. Importantly, . Dio2 expression in the EC is suppressed on day 1 after the onset of injection, whereas . TSH-β expression in the PT was not suppressed until day 10. These data suggest that regulated transcription of . TSH-β is involved in the induction of the gonadal axis in mammals, whereas the suppression of this axis is mediated by different mechanisms.

Original languageEnglish
Pages (from-to)43-50
Number of pages8
JournalJournal of Neuroendocrinology
Volume22
Issue number1
DOIs
Publication statusPublished - Jan 2010
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

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