Ootsuka Youichirou, McAllen Robin M
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia.
Am J Physiol Regul Integr Comp Physiol. 2006 Sep;291(3):R589-95. doi: 10.1152/ajpregu.00850.2005.
In cold defense and fever, activity increases in sympathetic nerves supplying both tail vessels and interscapular brown adipose tissue (iBAT). These mediate cutaneous vasoconstrictor and thermogenic responses, respectively, and both depend upon neurons in the rostral medullary raphé. To examine the commonality of brain circuits driving these two outflows, sympathetic nerve activity (SNA) was recorded simultaneously from sympathetic fibers in the ventral tail artery (tail SNA) and the nerve to iBAT (iBAT SNA) in urethane-anesthetized rats. From a warm baseline, cold-defense responses were evoked by intermittently circulating cold water through a water jacket around the animal's shaved trunk. Repeated episodes of trunk skin cooling decreased core (rectal) temperature. The threshold skin temperature to activate iBAT SNA was 37.3 +/- 0.5 degrees C (n = 7), significantly lower than that to activate tail SNA (40.1 +/- 0.4 degrees C; P < 0.01, n = 7). A fall in core temperature always strongly activated tail SNA (threshold 38.3 +/- 0.2 degrees C, n = 7), but its effect on iBAT SNA was absent (2 of 7 rats) or weak (threshold 36.9 +/- 0.1 degrees C, n = 5). The relative sensitivity to core vs. skin cooling (K-ratio) was significantly greater for tail SNA than for iBAT SNA. Spectral analysis of paired recordings showed significant coherence between tail SNA and iBAT SNA only at 1.0 +/- 0.1 Hz. The coherence was due entirely to the modulation of both signals by the ventilatory cycle because it disappeared when the coherence spectrum was partialized with respect to airway pressure. These findings indicate that independent central pathways drive cutaneous vasoconstrictor and thermogenic sympathetic pathways during cold defense.
在机体抵御寒冷和发热时，支配尾部血管和肩胛间棕色脂肪组织（iBAT）的交感神经活动增强。这些交感神经分别介导皮肤血管收缩反应和产热反应，且两者均依赖于延髓头端中缝核的神经元。为了研究驱动这两种传出神经活动的脑回路的共性，在乌拉坦麻醉的大鼠中，同时记录腹侧尾动脉交感神经纤维（尾部交感神经活动，tail SNA）和支配iBAT的神经（iBAT交感神经活动，iBAT SNA）的交感神经活动。从温暖的基线状态开始，通过围绕动物剃毛躯干的水套间歇性循环冷水来诱发机体的寒冷防御反应。反复的躯干皮肤冷却会降低核心（直肠）温度。激活iBAT SNA的阈值皮肤温度为37.3±0.5℃（n = 7），显著低于激活尾部SNA的阈值皮肤温度（40.1±0.4℃；P < 0.01，n = 7）。核心温度下降总是强烈激活尾部SNA（阈值38.3±0.2℃，n = 7），但其对iBAT SNA没有影响（7只大鼠中有2只）或影响较弱（阈值36.9±0.1℃，n = 5）。尾部SNA对核心温度与皮肤冷却的相对敏感性（K比值）显著高于iBAT SNA。对配对记录进行频谱分析显示，仅在1.0±0.1 Hz时，尾部SNA和iBAT SNA之间存在显著的相干性。这种相干性完全是由于通气周期对两种信号的调制所致，因为当相干性频谱相对于气道压力进行偏相关分析时，相干性消失。这些发现表明，在机体抵御寒冷期间，独立的中枢通路驱动皮肤血管收缩交感神经通路和产热交感神经通路。
