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Chemical sympathectomy with daily, intraperitoneal (IP) injections of guanethidine sulfate to adult rats, attenuated myenteric, but not dorsal vagal complex (DVC) Fos-like immunoreactivity (Fos-LI) by cholecystokinin-8 (CCK). This technique destroys only 60-70% of the sympathetic neurons, and spares the hormonal source of catecholamines, the adrenal medulla. The goal of the current study is to evaluate the effect of complete sympathectomy or destroying 100% of the sympathetic neurons by injecting guanethidine to 1-day-old pups (40 mg/kg daily for 5 weeks), and surgically removing the adrenal medulla. In the DVC, demedullation and sympathectomy-demedullation increased Fos-LI by CCK in the area postrema and nucleus of the solitary tract, but sympathectomy-demedullation increased it only in the area postrema. In the myenteric plexus, sympathectomy increased this response in the duodenum, and demedullation increased it in the duodenum and jejunum. On the other hand, sympathectomy-demedullation attenuated myenteric Fos-LI in the jejunum. These results indicate that catecholamines may play an inhibitory role on the activation of the DVC neurons by CCK. In the myenteric neurons, however, catecholamines may have both inhibitory and excitatory roles depending on the level of the intestine e.g., duodenum vs. jejunum. This may also indicate that CCK activates the enteric neurons by different mechanisms or through different pathways.

Vagotomy and capsaicin treatment attenuate dorsal vagal complex (DVC) but not myenteric Fos-like immunoreactivity (Fos-LI) induced by cholecystokinin-8 (CCK-8). The goal of this experiment is to test the role of the sympathetic nervous system in the pathway by which CCK-8 increases myenteric Fos-LI. Adult male Sprague-Dawley rats were pretreated with guanethidine sulfate (40 mg/kg daily for 5 weeks) or vehicle intraperitoneally (IP), and injected with CCK-8 (40 microg/kg) or saline IP. Fos-LI was then quantified in the DVC and the myenteric neurons of the duodenum and jejunum using a diaminobenzidine reaction. Guanethidine pretreatment attenuated myenteric but not DVC Fos-LI induced by CCK-8. These findings demonstrate that sympathetic neurons play a role in mediating the myenteric Fos-LI response to CCK. They also suggest differential mediation of myenteric and DVC responses to CCK.