TY - JOUR
T1 - Thyrotropin-releasing hormone increased heat production without the involvement of corticotropin-releasing factor in neonatal chicks
AU - Tachibana, Tetsuya
AU - Takahashi, Hirokazu
AU - Oikawa, Daichi
AU - Denbow, D. Michael
AU - Furuse, Mitsuhiro
N1 - Funding Information:
The authors are grateful to Momoka Sato, Shozo Tomonaga and Nami Adachi, Kyushu University, Japan, for their helps. This work was supported by Grant-in-Aid for Young Scientists (No. 15780187), Grant-in-Aid for Scientific Research from Japan Society for the Promotion of Science and Inamori Foundation.
PY - 2006/4
Y1 - 2006/4
N2 - Thyrotropin-releasing hormone (TRH) is a hypothalamic signal in the hypothalamic-pituitary-thyroid (HPT) axis, and is well known as a hyperthermic hormone in the brain of chicks. The thermogenetic effect leads to the hypothesis that central TRH increases heat production (HP) in chicks. The purpose of the present study was to clarify whether central TRH affects HP of neonatal chicks, and if such an effect is mediated by corticotropin-releasing factor (CRF) since the thermogenetic effect of TRH is mediated by CRF. Intracerebroventricular (ICV) injection of TRH (14 and 55 nmol) dose-dependently increased oxygen consumption, carbon dioxide production and HP, and a similar effect was also observed with CRF (2.1 and 21 pmol). The TRH-induced increase in HP could not be attenuated by astressin, a CRF receptor antagonist, while the effect of CRF was completely diminished by astressin. The present study demonstrates that central TRH increases HP in chicks but the effect was not related to CRF.
AB - Thyrotropin-releasing hormone (TRH) is a hypothalamic signal in the hypothalamic-pituitary-thyroid (HPT) axis, and is well known as a hyperthermic hormone in the brain of chicks. The thermogenetic effect leads to the hypothesis that central TRH increases heat production (HP) in chicks. The purpose of the present study was to clarify whether central TRH affects HP of neonatal chicks, and if such an effect is mediated by corticotropin-releasing factor (CRF) since the thermogenetic effect of TRH is mediated by CRF. Intracerebroventricular (ICV) injection of TRH (14 and 55 nmol) dose-dependently increased oxygen consumption, carbon dioxide production and HP, and a similar effect was also observed with CRF (2.1 and 21 pmol). The TRH-induced increase in HP could not be attenuated by astressin, a CRF receptor antagonist, while the effect of CRF was completely diminished by astressin. The present study demonstrates that central TRH increases HP in chicks but the effect was not related to CRF.
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U2 - 10.1016/j.pbb.2006.03.012
DO - 10.1016/j.pbb.2006.03.012
M3 - Article
C2 - 16624394
AN - SCOPUS:33744513919
VL - 83
SP - 528
EP - 532
JO - Pharmacology Biochemistry and Behavior
JF - Pharmacology Biochemistry and Behavior
SN - 0091-3057
IS - 4
ER -