Nitric oxide (NO) is shown to be synthesized in the central nervous system as well as in vascular endothelial cells. However, the physiological role of NO in cardiovascular regulation in the central nervous system remains unclear. The present study examines whether NO plays a role in the regulation of neuronal activity in the nucleus tractus solitarius (NTS). Single-unit extracellular recordings were obtained from NTS neurons in slices (400 μm) of the rat brainstem, which had spontaneous discharges at a frequency of 0.5 to 3 spikes per second. Eighty-one neurons were tested for sensitivity to L- arginine, which is the physiological precursor of NO. L-Arginine (10-7 to 10-4 mol/L) increased neuronal activity dose dependently in 33 (40.7%) of 81 neurons tested, but D-arginine (10-5 mol/L) did not. The neurons that responded to L-arginine responded to glutamate as well. N(G)-Monomethyl-L- arginine (10-5 to 3x10-5 mol/L), an inhibitor of the formation of NO, dose-dependently blocked increases in the neuronal activity evoked with L- arginine (10-5 mol/L). Hemoglobin (1.5 mg/L), a trapper of NO, and methylene blue (10-5 mol/L), an inhibitor of guanylate cyclase, also blocked increases in the neuronal activity evoked with L-arginine (10-5 mol/L). Sodium nitroprusside (SNP, 10-5 to 10-4 mol/L), which spontaneously produces NO, increased the neuronal activity in the neurons that responded to L-arginine. SNP did not alter the neuronal activity of the neurons that did not respond to L-arginine. Methylene blue (10-5 mol/L) blocked increases in the neuronal activity evoked with SNP (10-5 mol/L), but hemoglobin did not. These results suggest that NO is formed from L- arginine in the NTS neurons and that NO increases the neuronal activity of adjacent neurons in the NTS through an increase in cGMP.
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