Roles of central nicotinic receptors in regulation of gastric functions.

In the first part of this paper, the effects of single administration of nicotine on gastric motility of urethane-anesthetized rats are briefly summarized from our recently reported papers. Then, the effects of repeated administration of nicotine on the nicotine-induced changes in gastric motility and release of hypothalamic noradrenaline, in vitro, are described, with special references to up-regulation of nicotinic receptors. Nicotine 0.1 nmol administered into the dorsal motor nucleus of the vagus (DMV) elicited a dual change, a decrease followed by an increase in gastric motility. Intravenous administration of nicotine 300 nmol/kg decreased gastric motility. This decrease in gastric motility was inhibited by microinjection of hexamethonium into the DMV and was terminated by bilateral vagotomy. In animals pretreated with nicotine 200 nmol intracerebroventricularly (icv) administered once a day for 5 days, nicotine 100 nmol administered icv induced the decrease but not the increase in gastric motility. In conclusion, nicotine activates nicotinic receptors in the DMV and a resultant vagally-mediated dual change in gastric motility occurs. Furthermore, gastric inhibitory mechanisms in the DMV are susceptible to nicotine more than the excitatory mechanisms, and desensitization to nicotine occurs easily in the excitatory mechanisms.