Mazet B, Miolan J P, Niel J P, Roman C
Laboratoire de Neurophysiologie-Département de Physiologie et Neurophysiologie-URA CNRS 205 Faculté des Sciences et Techniques de St-Jérôme, Marseille, France.
J Auton Nerv Syst. 1994 Jan-Feb;46(1-2):135-46. doi: 10.1016/0165-1838(94)90150-3.
The mechanisms involved at the prevertebral ganglionic level in a gastroduodenal inhibitory reflex were investigated in the rabbit on an in vitro preparation of the coeliac plexus connected to the stomach and duodenum. Intraluminal gastric and duodenal pressures were measured using water-filled balloons. Gastric distension inhibited duodenal motility via a nerve reflex which was abolished by section of the nerves connecting the coeliac plexus to the viscera. Superfusion of the coeliac plexus with a low Ca(2+)-high Mg2+ solution abolished the gastroduodenal inhibitory reflex, indicating a synaptic link at the ganglion level. The reflex was unaffected by superfusion of the coeliac plexus with hexamethonium and tubocurarine, ruling out a nicotinic mechanism. The reflex persisted when the coeliac plexus was superfused with tetrodotoxin or when the nerves connecting the coeliac plexus to the viscera were superfused with a Na(+)-free solution; these results indicate that the reflex does not involve sodium-dependent action potentials. Moreover, superfusion of the nerves connecting the coeliac plexus to the viscera with a calcium blocker or with a Ca(2+)-free solution also failed to abolish the reflex, suggesting that calcium-dependent action potentials are not involved. Our study demonstrates that a gastrointestinal inhibitory reflex via the coeliac ganglion is not based on fast synaptic inputs or action potentials. These results provide new insights concerning the physiology of the sympathetic prevertebral ganglia.
