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The dorsomedial hypothalamus: a new player in thermoregulation.

机译:背侧下丘脑:体温调节的新角色。

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摘要

Neurons in the dorsomedial hypothalamus (DMH) play key roles in physiological responses to exteroceptive ("emotional") stress in rats, including tachycardia. Tachycardia evoked from the DMH or seen in experimental stress in rats is blocked by microinjection of the GABA(A) receptor agonist muscimol into the rostral raphe pallidus (rRP), an important thermoregulatory site in the brain stem, where disinhibition elicits sympathetically mediated activation of brown adipose tissue (BAT) and cutaneous vasoconstriction in the tail. Disinhibition of neurons in the DMH also elevates core temperature in conscious rats and sympathetic activity to least significant difference interscapular BAT (IBAT) and IBAT temperature in anesthetized preparations. The latter effects are blocked by microinjection of muscimol into the rRP, while microinjection of muscimol into either the rRP or DMH suppresses increases in sympathetic nerve activity to IBAT, IBAT temperature, and core body temperature elicited either by microinjection of PGE(2) into the preoptic area (an experimental model for fever), or central administration of fentanyl. Neurons concentrated in the dorsal region of the DMH project directly to the rRP, a location corresponding to that of neurons trans-synaptically labeled from IBAT. Thus these neurons control nonshivering thermogenesis in rats, and their activation signals its recruitment in diverse experimental paradigms. Evidence also points to a role for neurons in the DMH in thermoregulatory cutaneous vasoconstriction, shivering, and endocrine adjustments. These directions provide intriguing avenues for future exploration that may expand our understanding of the DMH as an important hypothalamic site for the integration of autonomic, endocrine, and behavioral responses to diverse challenges.
机译:背侧下丘脑(DMH)中的神经元在对大鼠(包括心动过速)的兴奋性(“情绪”)应激的生理反应中起关键作用。从DMH诱发或在大鼠实验压力下观察到的心动过速被GABA(A)受体激动剂麝香酚微注射到大脑中脑重要的温度调节位点rostral raphe pallidus(rRP)中,在那里抑制作用引起交感神经介导的激活褐色脂肪组织(BAT)和尾部皮肤血管收缩。 DMH中神经元的抑制作用还会使清醒大鼠的核心温度和交感活性升高至麻醉制剂中的肩cap间BAT(IBAT)和IBAT温度之间的差异最小。后一种作用通过向rRP中微量注射麝香酚而被阻滞,而向rRP或DMH中微量注射麝香酚则抑制了交感神经活性对IBAT,IBAT温度和通过将PGE(2)微量注射引起的核心体温的增加。视神经前区域(发烧的实验模型)或芬太尼的集中给药。集中在DMH背侧区域的神经元直接投射到rRP,该位置对应于从IBAT反式突触标记的神经元。因此,这些神经元控制了大鼠的不发抖的生热作用,并且它们的激活信号表明了其在各种实验范式中的募集。证据还表明,DMH中神经元在温度调节性皮肤血管收缩,发抖和内分泌调节中的作用。这些方向为将来的探索提供了有趣的途径,这些途径可能会扩展我们对DMH的理解,因为DMH是整合自主神经,内分泌和行为应对各种挑战的重要下丘脑部位。

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