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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
Author(s) -
Yasuo S.,
Yoshimura T.,
Ebihara S.,
Korf H.W.
Publication year - 2010
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2009.01936.x
Subject(s) - dio2 , pars tuberalis , medicine , endocrinology , deiodinase , biology , iodothyronine deiodinase , hormone , photoperiodism , triiodothyronine , pituitary gland
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.