Korsak A, Gilbey M P
Department of Physiology, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK.
Neuroscience. 2004;124(3):709-17. doi: 10.1016/j.neuroscience.2003.12.019.
Neurones within the rostral ventromedial medulla project to the intermediolateral cell column of the spinal cord where they may influence sympathetic preganglionic neuronal activity controlling cutaneous vascular beds. Here we assess whether such neurones contribute to cutaneous sympathetic vasoconstrictor activity in a fever-like state induced by i.c.v. injection of E-series prostaglandin. In urethane-anaesthetised rats, we recorded population sympathetic activity to the tail (an index of vasoconstrictor discharge regulating cutaneous thermoregulatory circulations). A survey of the effects of GABA microinjections (200 mM; 60-80 nl; 111 sites in 57 rats) demonstrated that those into the rostral ventromedial medulla (in the region of raphe pallidus and magnus; approximately bregma -10 to -12 mm) markedly decreased (51%-100%) population sympathetic cutaneous vasoconstrictor activity during "normothermic control." In contrast, injections at sites dorsal and lateral to this region tended to produce either a smaller decrease or have no effect. In heat-clamp (nine animals: body temperature 40-41 degrees C) cutaneous vasoconstrictor activity was decreased by 83+/-5%. I.c.v. prostaglandin E(1) (100 ng and above) restored activity to, or above, control levels in these animals and where body temperature was maintained at control levels (12 animals: body temperature 35.5-36.5 degrees C). The depressant action of GABA was sustained in both conditions. GABA did not significantly influence concurrently recorded splanchnic nerve activity and heart rate in any condition although both were increased following i.c.v. prostaglandin E(1) (500 ng). This study is the first to demonstrate that inhibition of neuronal activity within the rostral ventromedial medulla decreases sympathetic cutaneous vasoconstrictor activity during normothermic control and following i.c.v. prostaglandin E(1) (both with and without heat-clamp). Therefore, sympathetic premotor neurones in this area contribute to vasoconstrictor drive in these conditions. In contrast, we were unable to demonstrate that the same area had a substantial involvement in the control of splanchnic nerve activity or heart rate, even when these were enhanced following i.c.v. prostaglandin E(1).
延髓头端腹内侧的神经元投射至脊髓中间外侧细胞柱，在那里它们可能影响控制皮肤血管床的交感神经节前神经元活动。在此，我们评估此类神经元在脑室内注射E系列前列腺素诱导的发热样状态下是否参与皮肤交感缩血管活动。在乌拉坦麻醉的大鼠中，我们记录了对尾部的交感神经总体活动（调节皮肤体温调节循环的缩血管放电指标）。对γ-氨基丁酸（GABA）微量注射（200 mM；60 - 80 nl；57只大鼠中的111个位点）效应的调查表明，向延髓头端腹内侧（中缝苍白核和中缝大核区域；约前囟 -10至 -12 mm）的注射在“正常体温对照”期间显著降低（51% - 100%）交感神经总体皮肤缩血管活动。相比之下，在此区域背侧和外侧位点的注射往往产生较小的降低或无影响。在热钳制状态下（9只动物：体温40 - 41摄氏度），皮肤缩血管活动降低了83±5%。脑室内注射前列腺素E₁（100 ng及以上）使这些动物的活动恢复至对照水平或高于对照水平，以及在体温维持在对照水平的动物中（12只动物：体温35.5 - 36.5摄氏度）也是如此。在两种情况下，GABA的抑制作用均持续存在。在任何情况下，GABA均未显著影响同时记录的内脏神经活动和心率，尽管在脑室内注射前列腺素E₁（500 ng）后两者均增加。本研究首次表明，在正常体温对照期间以及脑室内注射前列腺素E₁后（无论有无热钳制），抑制延髓头端腹内侧的神经元活动会降低交感神经皮肤缩血管活动。因此，该区域的交感运动前神经元在这些情况下参与缩血管驱动。相比之下，我们未能证明同一区域在很大程度上参与内脏神经活动或心率的控制，即使在脑室内注射前列腺素E₁后这些活动增强时也是如此。
