Chida K, Iadecola C, Reis D J
Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.
Brain Res. 1990 Jan 29;508(1):93-104. doi: 10.1016/0006-8993(90)91122-w.
We sought to establish whether the C1 area of the rostral ventrolateral reticular nucleus (RVL) of the medulla oblongata mediates: (1) the elevations in arterial pressure (AP), heart rate (HR) and regional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral cerebellar fastigial nucleus (FN), the fastigial pressor response (FPR); (2) the reductions in AP and HR elicited by chemical stimulation of intrinsic neurons of FN with excitatory amino acids, the fastigial depressor response (FDR). Studies were conducted on rats anesthetized (chloralose), paralyzed and artificially ventilated. The FN was stimulated electrically through microelectrodes and chemically by microinjection of D.L-homocysteic acid (100 nmol in 100 nl). rCBF was measured in homogenates of 11 brain regions by the 14C-iodoantipyrine technique. Bilateral electrolytic lesions restricted to the RVL abolished the elevations in AP, HR and rCBF elicited by electrical stimulation as well as the fall of AP and HR elicited by chemical stimulation of the FN. The disappearance of the responses was anatomically selective and could not be attributed to changes in resting AP, HR or rCBF, loss of reactivity of preganglionic sympathetic neurons, or variations in blood gases. Since the FN neither projects to nor receives afferents from the RVL the pathway to RVL is indirect. We conclude that: (1) the FPR results from excitation and the FDR inhibition of reticulospinal sympathoexcitatory axons of RVL; (2) the FPR is a consequence of excitation of axons arising from neurons in an as yet unidentified area of lower brainstem projecting to or through the FN and with collateral branches innervating RVL mono- or polysynaptically; (3) the FDR, in contrast, represents excitation of intrinsic FN neurons with a polysynaptic projection to RVL through unidentified regions of lower brainstem; (4) the RVL is a relay mediating the increase in rCBF associated with the FPR; and (5) the RVL plays a critical role in integrating actions on the systemic and cerebral circulation represented in cerebellum.
我们试图确定延髓头端腹外侧网状核（RVL）的C1区是否介导：（1）电刺激小脑头端顶核（FN）所引起的动脉血压（AP）、心率（HR）和局部脑血流量（rCBF）升高，即顶核升压反应（FPR）；（2）用兴奋性氨基酸化学刺激FN的内在神经元所引起的AP和HR降低，即顶核降压反应（FDR）。研究在麻醉（氯醛糖）、麻痹并进行人工通气的大鼠身上进行。通过微电极对FN进行电刺激，并通过微量注射D.L-高半胱氨酸（100 nl中含100 nmol）进行化学刺激。采用14C-碘安替比林技术在11个脑区的匀浆中测量rCBF。局限于RVL的双侧电解损伤消除了电刺激所引起的AP、HR和rCBF升高，以及化学刺激FN所引起的AP和HR下降。反应的消失在解剖学上具有选择性，不能归因于静息AP、HR或rCBF的变化、节前交感神经元反应性的丧失或血气的变化。由于FN既不投射到RVL，也不接受来自RVL的传入纤维，因此到RVL的通路是间接的。我们得出以下结论：（1）FPR是由RVL的网状脊髓交感兴奋轴突的兴奋和FDR抑制引起的；（2）FPR是脑干下部一个尚未确定区域的神经元发出的轴突兴奋的结果，这些轴突投射到FN或通过FN，并具有侧支单突触或多突触地支配RVL；（3）相反，FDR代表FN内在神经元的兴奋，通过脑干下部未确定区域多突触地投射到RVL；（4）RVL是介导与FPR相关的rCBF增加的中继站；（5）RVL在整合小脑所代表的对全身和脑循环的作用中起关键作用。
