Expression of c-fos-like immunoreactivity in the feline brainstem in response to isometric muscle contraction and baroreceptor reflex changes in arterial pressure.
This study compared whether activation of muscle ergoreceptor afferents caused by isometric muscle contraction, activation of baroreceptor afferents induced by i.v. infusion of phenylephrine, or baroreceptor afferent inactivation, caused by carotid artery occlusion, elicit similar patterns of c-Fos induction in brainstem areas. Adult cats were anesthetized with alpha-chloralose, and in each case, the experimental intervention caused an increase in the arterial blood pressure. There were two sets of control experiments: in both, animals underwent the same surgical procedures but then either remained at rest for the entire study, or the tibial nerve was stimulated, as in the contraction group, following muscle paralysis with tubocurarine. Following the procedures, animals rested for 90 min to allow neuronal expression of c-Fos. Control cats showed very little c-Fos immunoreactivity (c-Fos-ir) in the brainstem. Muscle contraction induced c-Fos-ir expression mainly in the nucleus tractus solitarius, lateral reticular nucleus, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, spinal trigeminal tract and in a lateral region of the periaqueductal grey (P 0.5-1.0). The majority of the c-Fos-ir was found in brainstem areas contralateral to the contracted muscle. In addition, muscle contraction induced c-Fos-ir in the dorsal horns of spinal segments L6-S1 on the ipsilateral side of the spinal cord. Phenylephrine infusion caused c-Fos-ir expression in the nucleus tractus solitarius, spinal trigeminal tract, solitary tract, and dorsal motor nucleus of the vagus. No c-Fos-ir was apparent in the periaqueductal grey. Carotid occlusions induced c-Fos-ir expression in the area postrema, nucleus tractus solitarius, solitary tract, and spinal trigeminal tract. Expression was bilateral. Areas that exhibited c-Fos-ir correspond to sites previously reported to release various neuropeptides in response to muscle contraction or carotid occlusions. These results indicate that the exercise pressor reflex and baroreflex activate similar, but not completely identical, sites in the brainstem.
Williams
C A
CA
Department of Physiology, The James H. Quillen College of Medicine, East Tennessee State University, Johnson City 37614-0576, USA. williams@etsu.edu
Loyd
S D
SD
Hampton
T A
TA
Hoover
D B
DB
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D000906:Antibodies; D001794:Blood Pressure / Q000502:physiology*; D001933:Brain Stem / Q000098:blood supply / Q000737:chemistry / Q000502:physiology*; D002339:Carotid Arteries; D002415:Cats; D004558:Electric Stimulation; D005260:Female; D002546:Ischemic Attack, Transient / Q000503:physiopathology; D007537:Isometric Contraction / Q000502:physiology*; D003473:Neuromuscular Nondepolarizing Agents / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000096:biosynthesis* / Q000276:immunology; D012018:Reflex / Q000502:physiology; D013566:Sympathomimetics / Q000494:pharmacology; D013979:Tibial Nerve / Q000502:physiology; D014403:Tubocurarine / Q000494:pharmacology
D000906:Antibodies; D003473:Neuromuscular Nondepolarizing Agents; D016760:Proto-Oncogene Proteins c-fos; D013566:Sympathomimetics; D010656:Phenylephrine; D014403:Tubocurarine