Morrison S F
Department of Physiology (M211), Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Ann N Y Acad Sci. 2001 Jun;940:286-98. doi: 10.1111/j.1749-6632.2001.tb03684.x.
The medullary premotor neurons determining the sympathetic outflow regulating cardiac function and vasoconstriction are located in the rostral ventrolateral medulla (RVLM). The present study sought evidence for differential characteristics and baroreceptor reflex sensitivities between the sympathetic nerve activity (SNA) controlling brown adipose tissue (BAT) metabolism and thermogenesis and cardiovascular SNA such as that controlling mesenteric vasoconstriction via the splanchnic (SPL) nerve. The tonic discharge of sympathetic nerves is determined by the inputs to functionally specific sympathetic preganglionic neurons from supraspinal populations of premotor neurons. Under normothermic conditions, BAT SNA was nearly silent, while SPL SNA exhibited sustained, large-amplitude bursts. Disinhibition of neurons in the rostral raphe pallidus (RPa), a potential site of sympathetic premotor neurons controlling BAT SNA, or icv injection of prostaglandin E2, a pyrogenic stimulus, elicited a dramatic increase in BAT SNA. SPL SNA was strongly influenced by the baroreceptor reflex as indicated by a high coherence to the arterial pressure, while activated BAT SNA exhibited no correlation with the arterial pressure. Since these characteristics and reflex responses in sympathetic outflow have been shown to arise from the ongoing or altered discharge of sympathetic premotor neurons, the marked differences between SPL SNA and BAT SNA provide strong evidence supporting the hypothesis that vasoconstriction and thermogenesis (metabolism) are controlled by distinct populations of sympathetic premotor neurons, the former in the RVLM and strongly baroreceptor-modulated and the latter potentially in the RPa exhibiting little influence of baroreceptor reflex activation.
决定调节心脏功能和血管收缩的交感神经输出的延髓前运动神经元位于延髓头端腹外侧（RVLM）。本研究旨在寻找证据，以证明控制棕色脂肪组织（BAT）代谢和产热的交感神经活动（SNA）与心血管SNA（如通过内脏神经（SPL）控制肠系膜血管收缩的SNA）之间存在不同特征和压力感受器反射敏感性。交感神经的紧张性放电由运动前神经元的脊髓上群体对功能特异性交感神经节前神经元的输入所决定。在常温条件下，BAT SNA几乎处于静息状态，而SPL SNA则表现出持续的大幅度爆发。对延髓头端中缝苍白核（RPa）中的神经元进行去抑制（RPa是控制BAT SNA的交感神经运动前神经元的潜在部位），或脑室内注射前列腺素E2（一种致热刺激物），可使BAT SNA显著增加。如与动脉压的高相干性所示，SPL SNA受压力感受器反射的强烈影响，而激活的BAT SNA与动脉压无相关性。由于交感神经输出中的这些特征和反射反应已被证明源于交感神经运动前神经元的持续或改变的放电，SPL SNA和BAT SNA之间的显著差异提供了有力证据，支持以下假设：血管收缩和产热（代谢）由不同群体的交感神经运动前神经元控制，前者位于RVLM且受压力感受器强烈调节，后者可能位于RPa，几乎不受压力感受器反射激活的影响。
