NaCN is a classical stimulus used to elicit discharges from carotid body ch
emoreceptors. The effect is assumed to be mediated by glomus (type I) cells
, which release an excitatory transmitter for the excitation of carotid ner
ve endings. Since the sensory perikarya of the glossopharyngeal nerve (from
which the carotid nerve branches) are located in the petrosal ganglion, we
tested whether application of this drug to the petrosal ganglion superfuse
d in vitro elicits antidromic discharges in the carotid nerve. NaCN did ind
eed cause an intense and prolonged burst of nerve impulses in the carotid n
erve, while provoking a less intense and much briefer burst of discharges i
n the glossopharyngeal branch. Carotid nerve responses to NaCN were reduced
and shortened by prior or following application of dopamine to the ganglio
n. Sodium azide applied to the petrosal ganglion evoked a less intense and
much briefer burst of impulses in the carotid nerve. Ganglionar application
of 2,4-dinitrophenol did not induce discharges in the carotid nerve. Switc
hing the superfusion of the ganglion from a normoxic to a hypoxic solution
did not evoke discharges in the carotid nerve. Therefore, the perikarya of
carotid nerve neurons are sensitive to NaCN, but are not excited by reducin
g the pO(2) of the superfusing solution. (C) 1999 Elsevier Science B.V. All
rights reserved.