Recent findings suggest that carotid chemoreceptor input into the vent
ral medullary surface intermediate area during hypoxia is inhibitory (
Gozal et al., (1994) Neurosci. Lett. 178, 73-76. However, systemic hyp
oxia is a complex stimulus, and effects of carotid chemoreceptor stimu
lation per se on intermediate ventral medullary surface neuronal activ
ity are difficult to isolate. Therefore, we studied neural activation
of the intermediate ventral medullary surface during peripheral chemor
eceptor stimulation by intravenous sodium cyanide using optical proced
ures in seven pentobarbital-anesthetized cats. Control recordings were
also acquired in the suprasylvian cortex of three cats. Images of ref
lected 660 nm light were collected at 1/s with a charge-coupled device
camera, triggered by the cardiac R wave, after 0.0, 0.5, 2, 5, 10, 20
and 40 mu g/kg i.v. sodium cyanide administration before and followin
g carotid sinus denervation. Sodium cyanide doses > 5 mu g/kg signific
antly increased ventilation, an effect which was eliminated following
carotid sinus denervation. A pronounced, dose-dependent activity decre
ase within the intermediate ventral medullary surface occurred within
seconds of sodium cyanide administration, with subsequent return to ba
seline. Carotid sinus denervation eliminated rapid-onset neural respon
ses to all sodium cyanide doses. However, at the 40 mu g/kg dose, a sm
aller, slower onset (25 s), activity decrease occurred both pre- and p
ostdenervation. In the neocortex, the sodium cyanide-induced fast resp
onses were absent. Intravenous cyanide, acting via a carotid sinus ner
ve pathway, results in a dose-dependent decrease in neural activity wi
thin the intermediate ventral medullary surface of cats. High-dose sod
ium cyanide also appears to decrease intermediate ventral medullary su
rface neural activity directly. Copyright (C) 1996 IBRO.