Lesions of rostral ventrolateral medulla abolish some cardio- and cerebrovascular components of the cerebellar fastigial pressor and depressor responses

• Published in: Brain research Vol. 508; no. 1; p. 93
• Main Authors: Chida, K, Iadecola, C, Reis, D J
• Format: Journal Article
• Language: English
• Published: Netherlands 01.01.1990
• Subjects: Animals; Blood Pressure - drug effects; Cardiovascular Physiological Phenomena; Cardiovascular System - drug effects; Cerebellar Nuclei - physiology; Cerebrovascular Circulation; Electric Stimulation; Heart Rate - drug effects; Male; Medulla Oblongata - physiology; Phenylephrine - pharmacology; Rats; Rats, Inbred Strains
• ISSN: 0006-8993
• 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.