The present study analyses the expression and distribution of neuronal nitric oxide synthase (nNOS) in the brainstem of animals pre-treated with Escherichia coli or Helicobacter pylori LPS, at doses that modulate gastric motor function. Systemic administration of H. pylori LPS prevented in a dose-dependent manner (5, 40 and 100 microg kg(-1), i.v.) the increase in intragastric pressure induced by 2-deoxy-D-glucose (200 mg kg(-1), i.v.) in urethane-anaesthetized rats. Quantitative analysis showed a significant increase in the amount of nNOS mRNA induced by E. coli or H. pylori LPS (2 h later), in a segment of the brainstem containing the dorsal vagal complex (DVC). Immunohistochemical studies showed nNOS presence in the DVC of vehicle-treated rats. Both E. coli (40 microg kg(-1), i.p.) and H. pylori LPS (100 microg kg(-1), i.p.) significantly increased (2 h later) the number of nNOS immunoreactive cells in this area, mainly at the most rostral level. The present study shows that systemic administration of E. coli or H. pylori LPS induces a transcriptional up-regulation of the nNOS in the DVC of the brainstem and suggests a role for NO synthesis in this area in the control of gastric motor function under endotoxemia.