Lam W, Verberne A J
University of Melbourne, Department of Medicine, Austin and Repatriation Medical Centre, Heidelberg, Australia.
Brain Res. 1997 May 23;757(2):191-201. doi: 10.1016/s0006-8993(97)00201-1.
Stimulation of the midbrain cuneiform nucleus has previously been shown to produce increases in arterial blood pressure and lumbar sympathetic nerve activity. While this sympathoexcitatory effect is, in part, due to excitation of premotor sympathoexcitatory neurons in the rostral ventrolateral medulla, the specific spinal neurotransmitter systems recruited by cuneiform nucleus stimulation remains to be elucidated. In this study, mean arterial pressure, resting and cuneiform nucleus stimulation-evoked lumbar sympathetic nerve activity were analysed following intrathecal injections of an excitatory amino acid antagonist (kynurenic acid), alpha1-adrenoceptor antagonist (prazosin) and a serotonin receptor antagonist (methiothepin) in anesthetized, paralysed male Sprague-Dawley rats. Mean arterial pressure and resting sympathetic nerve discharge were decreased by all treatments (n = 6/group) compared to the vehicle control group. Intermittent electrical stimulation of the cuneiform nucleus produced a bimodal sympathoexcitatory response, of which the short latency peak was significantly attenuated (43% reduction) by intrathecal kynurenate whereas the long latency peak was reduced by intrathecal prazosin (decrease of 21%) and methiothepin (38% attenuation). These results are consistent with the significant roles of excitatory amino acid, alpha1-adrenergic and serotonin receptors in modulating the activity of sympathetic vasomotor preganglionic neurons supplying the lumbar sympathetic nerve trunk, and suggest the existence of at least three neuronal groups and/or pathways associated with the sympathoexcitatory response to cuneiform nucleus stimulation.
先前的研究表明,刺激中脑楔形核会导致动脉血压升高和腰交感神经活动增强。虽然这种交感神经兴奋作用部分归因于延髓头端腹外侧部运动前交感神经兴奋神经元的兴奋,但楔形核刺激所募集的特定脊髓神经递质系统仍有待阐明。在本研究中,对麻醉、麻痹的雄性Sprague-Dawley大鼠进行鞘内注射兴奋性氨基酸拮抗剂(犬尿喹啉酸)、α1-肾上腺素能受体拮抗剂(哌唑嗪)和5-羟色胺受体拮抗剂(甲硫噻平)后,分析平均动脉压、静息和楔形核刺激诱发的腰交感神经活动。与溶剂对照组相比,所有处理(每组n = 6)均使平均动脉压和静息交感神经放电降低。间歇性电刺激楔形核产生双模式交感神经兴奋反应,其中鞘内注射犬尿酸可使短潜伏期峰值显著减弱(降低43%),而鞘内注射哌唑嗪(降低21%)和甲硫噻平(减弱38%)可使长潜伏期峰值降低。这些结果与兴奋性氨基酸、α1-肾上腺素能和5-羟色胺受体在调节供应腰交感神经干的交感血管运动节前神经元活动中的重要作用一致,并提示至少存在三个与楔形核刺激交感神经兴奋反应相关的神经元群和/或通路。