Nitric oxide released by gastric mechanoreceptors modulates nicotinic activation of coeliac plexus neurons in the rabbit.

The effects on the nicotinic activation of the coeliac plexus neurons of nitric oxide (NO) released within the coeliac plexus by gastric mechanoreceptors, in particular during gastroduodenal inhibitory reflex, were assessed. This study was performed in the rabbit on an in vitro preparation of the coeliac plexus connected to the stomach and the duodenum. The electrical activity of ganglionic neurons was recorded with intracellular recording techniques. Water-filled balloons were used for gastric distensions and recording of duodenal motility. When a 10-s train of pulses (20-40Hz) of supramaximal intensity was applied to the splanchnic nerves, gradual depression of nicotinic activation occurred. Gastric distension (50 mL, 7.5 min) modulated this depression phenomenon by inhibiting or facilitating the nicotinic activation. In the neurons impaled during the recording of duodenal motility, gastric distension triggered an inhibition of nicotinic activation concomitantly with a gastroduodenal inhibitory reflex organized by the coeliac plexus. If the gastric distensions were performed while the coeliac plexus was superfused by a NO scavenger, the nicotinic activation was unaffected and the gastroduodenal inhibitory reflex was abolished. Moreover, when the coeliac plexus was superfused with an inhibitor of nitric oxide synthase, gastric distensions were without effect on the nicotinic activation. These results demonstrate that NO released within the coeliac plexus by gastric mechanoreceptors, in particular during the gastroduodenal inhibitory reflex, modulates the central nicotinic activation of coeliac plexus neurons, so NO released within a prevertebral ganglion by gastric afferent fibres, in particular during the organization by this ganglion of a reflex regulating the gastrointestinal tract motility, also exerts a gating of the central inputs to the ganglionic neurons.