title: Ventral medullary neuronal responses to peripheral chemoreceptor stimulation.
abstract: Recent findings suggest that carotid chemoreceptor input into the ventral medullary surface intermediate area during hypoxia is inhibitory (Gozal et al., (1994) Neurosci. Lett. 178, 73-76. However, systemic hypoxia is a complex stimulus, and effects of carotid chemoreceptor stimulation per se on intermediate ventral medullary surface neuronal activity are difficult to isolate. Therefore, we studied neural activation of the intermediate ventral medullary surface during peripheral chemoreceptor stimulation by intravenous sodium cyanide using optical procedures in seven pentobarbital-anesthetized cats. Control recordings were also acquired in the suprasylvian cortex of three cats. Images of reflected 660 nm light were collected at l/s with a charge-coupled device camera, triggered by the cardiac R wave, after 0.0, 0.5, 2, 5, 10, 20 and 40 micrograms/kg i.v. sodium cyanide administration before and following carotid sinus denervation. Sodium cyanide doses > 5 micrograms/kg significantly increased ventilation, an effect which was eliminated following carotid sinus denervation. A pronounced, dose-dependent activity decrease within the intermediate ventral medullary surface occurred within seconds of sodium cyanide administration, with subsequent return to baseline. Carotid sinus denervation eliminated rapid-onset neural responses to all sodium cyanide doses. However, at the 40 micrograms/kg dose, a smaller, slower onset (25 s), activity decrease occurred both pre- and postdenervation. In the neocortex, the sodium cyanide-induced fast responses were absent. Intravenous cyanide, acting via a carotid sinus nerve pathway, results in a dose-dependent decrease in neural activity within the intermediate ventral medullary surface of cats. High-dose sodium cyanide also appears to decrease intermediate ventral medullary surface neural activity directly.
authors.affiliation: Division of Pediatric Pulmonology, Johns Hopkins Children's Center, Johns Hopkins School of Medicine, Baltimore, MD 21287-2533, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Carroll
authors.forename: D
authors.initials: D
authors.lastname: Gozal
authors.forename: D M
authors.initials: DM
authors.lastname: Rector
authors.forename: G
authors.initials: G
authors.lastname: Aljadeff
authors.forename: R M
authors.initials: RM
authors.lastname: Harper
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000294:innervation; D002415:Cats; D002540:Cerebral Cortex / Q000187:drug effects; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D003714:Denervation; D005260:Female; D006321:Heart / Q000187:drug effects; D008297:Male; D008526:Medulla Oblongata / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D055095:Optics and Photonics; D012119:Respiration / Q000187:drug effects; D012966:Sodium Cyanide / Q000494:pharmacology; D014628:Vagotomy
chemical_list: D012966:Sodium Cyanide