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饲养温度降低会增强交感神经对棕色脂肪组织的输出反应。

Reduced rearing temperature augments responses in sympathetic outflow to brown adipose tissue.

作者信息

Morrison S F, Ramamurthy S, Young J B

机构信息

Department of Physiology, Northwestern University Medical School, Chicago, Illinois 60611, USA.

出版信息

J Neurosci. 2000 Dec 15;20(24):9264-71. doi: 10.1523/JNEUROSCI.20-24-09264.2000.

Abstract

Sympathetic outflow to brown adipose tissue (BAT) contributes to both thermoregulation and energy expenditure in rats through regulation of BAT thermogenesis. Acute cold exposure in mature animals augments BAT thermogenesis; however, the enhanced BAT thermogenic response returns to normal shortly after cessation of the cold exposure. In this study, we sought to determine whether cold exposure in early neonatal life could induce enhanced responses in the sympathetic outflow to BAT and whether this altered sympathetic regulation would be sustained after the cold stimulus was removed. BAT sympathetic nerve activity (SNA) was recorded in urethane-chloralose-anesthetized, artificially ventilated rats that were raised from birth in either 18 or 30 degrees C environments and then, at 8 weeks of age, were maintained in 23 degrees C for at least 4 weeks. An acute hypothermic stimulus, disinhibition of a brainstem thermogenic network in the raphe pallidus, or electrical stimulation in this raphe site produced increases in BAT SNA that were twice as great in rats reared at 18 degrees C as in those reared at 30 degrees C. The norepinephrine content of the interscapular BAT (IBAT) and the number of sympathetic ganglion cells projecting to interscapular BAT were 70% greater in the 18 degrees C-reared rats. We conclude that neonatal exposure to a cold environment induces a permanent developmental alteration in the capacity for sympathetic stimulation of BAT thermogenesis that may be mediated, in part, by a greater number of sympathetic ganglion cells innervating BAT in cold-reared animals.

摘要

交感神经向棕色脂肪组织(BAT)的输出通过调节BAT产热,对大鼠的体温调节和能量消耗均有贡献。成熟动物急性暴露于寒冷环境会增强BAT产热;然而,在寒冷暴露停止后不久,增强的BAT产热反应会恢复正常。在本研究中,我们试图确定新生儿早期暴露于寒冷环境是否会诱导交感神经向BAT输出的反应增强,以及在去除寒冷刺激后,这种改变的交感神经调节是否会持续存在。在氨基甲酸乙酯-氯醛糖麻醉、人工通气的大鼠中记录BAT交感神经活动(SNA),这些大鼠从出生起就饲养在18或30摄氏度的环境中,然后在8周龄时,在23摄氏度下饲养至少4周。急性低温刺激、中缝苍白核脑干产热网络的去抑制或该中缝部位的电刺激,使饲养在18摄氏度的大鼠BAT SNA增加量是饲养在30摄氏度大鼠的两倍。饲养在18摄氏度的大鼠肩胛间BAT(IBAT)中的去甲肾上腺素含量以及投射到肩胛间BAT的交感神经节细胞数量比饲养在30摄氏度的大鼠多70%。我们得出结论,新生儿期暴露于寒冷环境会诱导BAT产热的交感神经刺激能力发生永久性发育改变,这可能部分是由寒冷饲养动物中支配BAT的交感神经节细胞数量增加介导的。

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