title: Trigeminal autonomic pathways involved in nociception-induced reflex cardiovascular responses.
abstract: Reflex cardiovascular responses elicited by noxious oro-facial stimulation are well known but the neural pathways that underlie trigeminal cardiovascular reflex reactions remain to be elucidated. In previous studies, we have shown that noxious electrical stimulation of the mandibular incisor in the anesthetized rat elicits increases in mean arterial blood pressure and heart rate (Allen, G.V., Barbrick, B. and Esser, M.J., Trigeminal parabrachial connections: possible pathway for nociception-induced cardiovascular reflex responses, Brain Res., 715 (1996) 125-135). In this study, microinjections of the presynaptic blocker, cobalt chloride, or the anesthetic agent, lidocaine, were made into selected brainstem sites to identify neural pathways that are involved in mediation of the reflex pressor responses. Ipsilateral and bilateral injections of chemical blocker into the dorsomedial spinal trigeminal nucleus, pars caudalis, lateral parabrachial nucleus and the rostral ventral lateral medulla/caudal A5 region attenuated the reflex cardiovascular response. Bilateral injections of cobalt chloride into the dorsomedial subnucleus caudalis resulted in 70-100% attenuation of the reflex pressor response. Bilateral injections of cobalt chloride and/or lidocaine into the lateral parabrachial nucleus or the rostral ventral lateral medulla/A5 region resulted in 43-57% and 44-100% attenuation of the reflex pressor response, respectively. There were no significant differences in the degree or duration of attenuation of the reflex pressor responses produced by cobalt chloride compared to that produced by lidocaine injections. The reflex pressor responses usually returned to baseline levels approximately 60 min following injection of the chemical blocker substance. The results indicate that noxious electrical stimulation of the mandibular incisor elicits a reflex increase in mean arterial blood pressure which is initially mediated in the dorsomedial spinal trigeminal nucleus, pars caudalis and is subsequently mediated in the lateral parabrachial nucleus and the rostral ventral lateral medulla/caudal A5 region.
authors.affiliation: Department of Anatomy and Neurobiology, Dalhousie University, Faculty of Medicine, Halifax, NS, Canada. gva@is.dal.ca
authors.forename: G V
authors.initials: GV
authors.lastname: Allen
authors.forename: S P
authors.initials: SP
authors.lastname: Pronych
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D003035:Cobalt / Q000008:administration & dosage / Q000494:pharmacology; D004558:Electric Stimulation; D007839:Functional Laterality; D006339:Heart Rate / Q000187:drug effects; D007180:Incisor / Q000294:innervation; D008012:Lidocaine / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D008340:Mandibular Nerve / Q000502:physiology; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D008959:Models, Neurological; D010146:Pain / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012018:Reflex; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D014279:Trigeminal Nucleus, Spinal / Q000502:physiology*
chemical_list: D003035:Cobalt; D008012:Lidocaine; C018021:cobaltous chloride