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首页> 外文期刊>Brain research >Thyrotropin-releasing hormone induced thermogenesis in Syrian hamsters: site of action and receptor subtype.
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Thyrotropin-releasing hormone induced thermogenesis in Syrian hamsters: site of action and receptor subtype.

机译：促甲状腺激素释放激素在叙利亚仓鼠中引起生热：作用部位和受体亚型。

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Early work in our laboratory has revealed the important role played by thyrotropin-releasing hormone (TRH) in the arousal from hibernation in Syrian hamsters. In the present study, we investigated the thermogenic mechanism of TRH in Syrian hamsters. Six to 10 female Syrian hamsters were used in the respective experiments. Intracerebroventricular (icv) injection of TRH elevated the intrascapular brown adipose tissue (IBAT) temperature (T(IBAT)) and rectal temperature (T rec) in Syrian hamsters. Thermogenic response of icv TRH was suppressed by bilateral denervation of the sympathetic nerve. Icv injection of TRH increased the norepinephrin (NE) turnover rate in IBAT without affecting the total serum triiodothyronine (T3) level. Moreover, TRH microinjections into the dorsomedial hypothalamus (DMH), preoptic area (PO), anterior hypothalamus (AH) and ventromedial hypothalamus (VMH) induced T(IBAT) and T(rec) increases. However, neither T(IBAT) nor T rec was affected by similar TRH administrations into the lateral hypothalamus and posterior hypothalamus. Interestingly, although TRH-induced hyperthermia was suppressed by pretreatment of anti-TRH-R1 antibodies, no changes were induced by anti-TRH-R2 antibodies. These results suggest that the sites of action of TRH associated with thermogenesis are probably localized in the DMH, PO, AH and VMH. In addition, TRH-induced thermogenesis is probably elicited by facilitation of the sympathetic nerve system via the central TRH-R1 irrelevant of T3.
机译：我们实验室的早期工作表明，促甲状腺素释放激素（TRH）在叙利亚仓鼠冬眠引起的唤醒中起着重要作用。在本研究中，我们调查了TRH在叙利亚仓鼠中的产热机理。在各自的实验中使用了六到十只雌性叙利亚仓鼠。脑室内（icv）注射TRH使叙利亚仓鼠的肩cap骨内棕色脂肪组织（IBAT）温度（T（IBAT））和直肠温度（T rec）升高。交感神经的双神经支配抑制了icv TRH的产热反应。静脉注射TRH可增加IBAT中去甲肾上腺素（NE）的转换率，而不会影响总血清三碘甲状腺素（T3）的水平。此外，TRH显微注射到背膜下丘脑（DMH），视前区（PO），下丘脑前部（AH）和腹膜下丘脑（VMH）诱导的T（IBAT）和T（rec）增加。然而，T（IBAT）和T rec均不受下丘脑外侧和后丘脑类似TRH给药的影响。有趣的是，尽管TRH诱导的高温被抗TRH-R1抗体的预处理所抑制，但抗TRH-R2抗体并未引起任何变化。这些结果表明，与生热相关的TRH的作用位点可能位于DMH，PO，AH和VMH中。此外，TRH诱导的生热可能是通过经由与T3无关的中央TRH-R1促进交感神经系统而引起的。

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