Modulatory effect of nitric oxide on acetylcholine-induced activation of cat petrosal ganglion neurons in vitro

The inhibitory effect of nitric oxide (NO) on carotid chemosensory responses to hypoxia has been attributed in part to an antidromic inhibition of chemoreceptor cells activity. However, NO may also modulate the activity of the primary sensory neurons because NO is produced in the soma of these neurons located in the petrosal ganglion. Since a population of petrosal neurons is selectively activated by acetylcholine (ACh), we studied the effects of NO-donor, sodium nitroprusside (SNP), and the NO-synthase inhibitor, Nω-nitro- l -arginine methyl ester ( l -NAME), on the responses evoked in the carotid sinus nerve (CSN) by ACh applied to the petrosal ganglion in vitro. ACh (1 μg–1 mg) increased the frequency of action potentials recorded from the CSN in a dose-dependent manner. SNP (10–50 μM) reduced the sensibility and amplitude of the CSN response to ACh, although the maximal response appears less affected. The withdrawal of SNP from the superfusion medium increased the sensibility of the responses to ACh. l -NAME (1–2 mM) slightly increased the sensibility of the ACh-induced responses, effect that persisted after l -NAME withdrawal. These results suggest that NO may play a role as modulator in this autonomic primary sensory ganglion.