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.
