Vagus nerve participates in CCK-induced Fos expression in hindbrain but not myenteric plexus.

CCK activates neurons in rat hindbrain and small intestinal myenteric ganglia. Activation of neurons at both sites is mediated through type A CCK receptors. CCK-induced activation of hindbrain neurons is mediated by capsaicin-sensitive vagal fibers. Therefore, it is possible that CCK-induced activation of myenteric neurons also depends upon vagal activation. To test this hypothesis, we examined hindbrain and myenteric neuronal expression of Fos immunoreactivity following CCK injection in rats that had undergone bilateral subdiaphragmatic vagotomy or systemic treatment with capsaicin, a neurotoxin that destroys small unmyelinated primary sensory neurons in the vagus, as well as in other peripheral nerves. We found that CCK (2 or 10 microg/kg) significantly increased Fos expression in both the brains and small intestinal myenteric plexuses of control rats. CCK-induced Fos expression was abolished or attenuated in the brains of vagotomized or capsaicin-treated animals. However, vagotomy or capsaicin treatment did not diminish CCK-induced Fos expression in the small intestinal myenteric plexus. We conclude that CCK-induced activation of intestinal myenteric neurons does not depend on activation of vagal sensory or motor neurons, while activation of neurons in the dorsal hindbrain is mediated, at least in part by CCK-induced activity of small unmyelinated vagal sensory neurons.