REGULATION OF CBF BY THE ROSTRAL VENTROLATERAL MEDULLA

描述延髓头端腹外侧（RVL）神经元的兴奋 提高大脑皮层内的局部脑血流量（rCBF） 而不会提高大脑的新陈代谢 这些神经元也介导了 脑血管舒张至缺氧。 三项研究将 在麻醉大鼠中进行，其中rCBF（通过激光多普勒血流仪） 并测量脑电图 研究1测试了以下假设：（a） 介导脑血管舒张的RVL在地形学上是 与网状脊髓交感神经元不同， 前者定位于尾侧（RVLc），后者定位于吻侧（RVLr）亚区， （B）氧检测神经元定位于RVLr但兴奋， 在髓内通路上，RVLc中的神经元升高rCBF;和（C） RVLc神经元还介导皮层电活动的同步化 通过电和化学刺激束核引起的 孤雌虫属（NTS）。 研究II使用解剖示踪技术结合 与病变和诱发活动的电生理记录：（a） 建立RVLc传出投射的靶点， 脑血管扩张，集中在神经元 中线-板内丘脑、齿状回和背侧下丘脑;和（B） 通过逆行标记确定投射到皮质的部位， 由RVL支配，当刺激RVL时，RVL将升高rCBF，当刺激RVL时，RVL将升高rCBF。 中断，将阻断RVLc引起的血管舒张。 研究III试验 假设一个特定的皮质神经元亚群， 氧敏感的，总是由神经性传入兴奋， 血管舒张部位，包括RVL，因此， 神经元活动转化为血管舒张。 神经元将被识别为 细胞外和细胞内染色， 通过光学显微镜观察形态学和大脑 微循环

DESCRIPTION Excitation of neurons of the rostral ventrolateral medulla (RVL) elevates regional cerebral blood flow (rCBF) within the cerebral cortex without elevating cerebral metabolism. These neurons also mediate half of the cerebrovascular vasodilatation to hypoxia. Three studies will be undertaken in anesthetized rats in which rCBF (by laser-Doppler flowmetry) and EEG will be measured. Study 1 tests the hypotheses that (a) neurons in RVL which mediate the cerebrovascular vasodilation are topographically distinct from the reticulo-spinal sympathoexcitatory neurons, with the former localized to caudal (RVLc) and the latter to rostral (RVLr) subareas, respectively; (b) oxygen detecting neurons are localized to RVLr but excite, over an intramedullary pathway, neurons in RVLc to elevate rCBF; and (C) neurons of RVLc also mediate the synchronization of electrocortical activity elicited by electrical and chemical stimulation of the nucleus tractus solitarii (NTS). Study II uses anatomical tracer techniques in conjunction with lesions and electrophysiological recording of evoked activity to: (a) establish the targets of efferent projections from RVLc which might mediate the cerebrovascular vasodilation, focusing on neurons of midline-intralaminar thalamus, zona incerta and dorsal hypothalamus; and (b) determine, by retrogradely labeling, sites projecting to the cortex and innervated by RVL, which, when stimulated, will elevate rCBF and, when interrupted, will block the vasodilation elicited by RVLc. Study III tests the hypothesis that a specific subpopulation of cortical neurons, possible oxygen-sensitive, are invariably excited by neurogenic afferentation for vasodilatory sites, including RVL, and as a result transduce afferent neuronal activity into vasodilation. The neurons will be identified by extra- and intracellular staining and will be phenotypically characterized by light microscopy with respect to morphology and in relation to cerebral microcirculation.