Tachibana Tetsuya, Takahashi Hirokazu, Oikawa Daichi, Denbow D Michael, Furuse Mitsuhiro
Laboratory of Advanced Animal and Marine Bioresources, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Fukuoka 812-8581, Japan.
Pharmacol Biochem Behav. 2006 Apr;83(4):528-32. doi: 10.1016/j.pbb.2006.03.012. Epub 2006 Apr 19.
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.
促甲状腺激素释放激素（TRH）是下丘脑-垂体-甲状腺（HPT）轴中的一种下丘脑信号，并且在雏鸡大脑中作为一种产热激素而广为人知。这种产热效应引发了一种假说，即中枢TRH会增加雏鸡的产热（HP）。本研究的目的是阐明中枢TRH是否会影响新生雏鸡的产热，以及如果存在这种效应，是否是由促肾上腺皮质激素释放因子（CRF）介导的，因为TRH的产热效应是由CRF介导的。脑室内（ICV）注射TRH（14和55 nmol）剂量依赖性地增加了氧气消耗、二氧化碳产生和产热，并且用CRF（2.1和21 pmol）也观察到了类似的效应。TRH诱导的产热增加不能被CRF受体拮抗剂阿斯特辛减弱，而CRF的效应被阿斯特辛完全消除。本研究表明，中枢TRH会增加雏鸡的产热，但这种效应与CRF无关。
