首页> 外文期刊>Brain research >Regulatory mechanism of body temperature in the central nervous system during the maintenance phase of hibernation in Syrian hamsters: involvement of β-endorphin.
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Regulatory mechanism of body temperature in the central nervous system during the maintenance phase of hibernation in Syrian hamsters: involvement of β-endorphin.

机译:叙利亚仓鼠冬眠维持阶段中枢神经系统体温的调节机制:β-内啡肽的参与。

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摘要

We have shown previously that intracerebroventricular (icv) injection of naloxone (a non-selective opioid receptor antagonist) or naloxonazine (a selective μ1-opioid receptor antagonist) at the maintenance phase of hibernation arouses Syrian hamsters from hibernation. This study was designed to clarify the role of β-endorphin (an endogenous μ-opioid receptor ligand) on regulation of body temperature (T(b)) during the maintenance phase of hibernation. The number of c-Fos-positive cells and β-endorphin-like immunoreactivity increased in the arcuate nucleus (ARC) after hibernation onset. In contrast, endomorphin-1 (an endogenous μ-opioid receptor ligand)-like immunoreactivity observed on the anterior hypothalamus decreased after hibernation onset. In addition, hibernation was interrupted by icv injection of anti-β-endorphin antiserum at the maintenance phase of hibernation. The mRNA expression level of proopiomelanocortin (a precursor of β-endorphin) on ARC did not change throughout the hibernation phase. However, the mRNA expression level of prohormone convertase-1 increased after hibernation onset. [D-Ala2,N-MePhe4,Gly-ol5] enkephalin (DAMGO, a selective μ-opioid receptor agonist) microinjection into the dorsomedial hypothalamus (DMH) elicited the most marked T(b) decrease than other sites such as the preoptic area (PO), anterior hypothalamus (AH), lateral hypothalamus (LH), ventromedial hypothalamus and posterior hypothalamus (PH). However, microinjected DAMGO into the medial septum indicated negligible changes in T(b). These results suggest that β-endorphin which synthesizes in ARC neurons regulates T(b) during the maintenance phase of hibernation by activating μ-opioid receptors in PO, AH, VMH, DMH and PH.
机译:先前我们已经证明,在冬眠维持阶段,脑室内(icv)注射纳洛酮(非选择性阿片受体拮抗剂)或纳洛酮嗪(选择性μ1-阿片受体拮抗剂)会引起叙利亚仓鼠冬眠。这项研究旨在阐明在维持休眠状态期间β-内啡肽(内源性μ阿片受体配体)在调节体温(T(b))中的作用。冬眠开始后,弓形核(ARC)中的c-Fos阳性细胞数量和β-内啡肽样免疫反应性增加。相比之下,冬眠开始后,在下丘脑前部观察到的endomorphin-1(内源性μ阿片受体配体)样免疫反应性降低。另外,在冬眠维持期,通过icv注射抗β-内啡肽抗血清中断冬眠。在整个冬眠阶段,弧菌中proopiomelanocortin(β-内啡肽的前体)的mRNA表达水平没有变化。但是,冬眠开始后原激素转化酶-1的mRNA表达水平增加。 [D-Ala2,N-MePhe4,Gly-ol5]脑啡肽(DAMGO,选择性μ阿片类受体激动剂)显微注射到下丘脑(DMH)引起的T(b)下降比其他部位如视前区明显(PO),下丘脑前(AH),下丘脑外侧(LH),腹侧下丘脑和后丘脑(PH)。但是,将DAMGO显微注射到内侧隔膜中,可观察到T(b)的变化可忽略不计。这些结果表明,在ARC神经元中合成的β-内啡肽在冬眠维持阶段通过激活PO,AH,VMH,DMH和PH中的μ阿片受体来调节T(b)。

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