PRESSOR EFFECTS OF ELECTRICAL-STIMULATION OF THE DORSAL AND MEDIAN RAPHE NUCLEI IN ANESTHETIZED RATS

Abstract

Electrical stimulation (1-50 Hz, 100-500 .mu.A, 0.3 ms pulse duration) of the dorsal or median raphe nucleus in anesthetized rats produces a transient increase in arterial blood pressure. Heart rate and respiratory rate do not appear to change systematically after stimulation. Transections rostral or caudal to the raphe nuclei or electrolytic lesions in the area of the nucleus linearis, pars caudalis abolishes the pressor response to stimulation. Depletion of brain serotonin with p-chlorophenylalanine significantly attenuates the pressor effects of both dorsal and median raphe stimulation. The p-chlorophenylalanine effect can be partially reversed by Ro 4-4602 [d-1-serine-N2-(2,3,4-trihydroxybenzyl)-hydrazide hydrochloride], a peripherally acting decarboxylase inhibitor, plus 5-hydroxytryptophan. Fluoxetine, a specific serotonin uptake inhibitor, prolongs the duration of the raphe pressor response and slightly increases its magnitude. Injections of 2-bromolysergic acid diethylamide (BOL), a putative serotonin antagonist, into the anterior hypothalamus/preoptic area significantly attenuates the dorsal raphe pressor effect, but treatment of rats with the sympathetic postganglionic blocking agent bretylium prevents the stimulation-induced pressor effect. Stimulation of the ascending serotonergic neuronal system produces a phasic pressor effect which is mediated by synaptic serotonin.