Nitric oxide synthase (NOS) and histamine H3 receptors are both markedly increased by neuronal injuries. To examine whether peripheral axotomy produced differential changes in NOS and H3 receptors, both NOS and H3 receptors were measured in the dorsal vagal complex after unilateral vagotomy. The presence of NOS-positive neurons was examined using both NADPH-diaphorase histochemistry and neuronal NOS-immunohistochemistry in rats vagotomized at the mid-cervical level. NADPH-diaphorase activity and NOS-immunoreactivity were markedly enhanced on the dorsal motor nucleus of the vagus (DMX) and in the ambiguus nucleus at the denervated side. Intraperitoneal injection of NOS inhibitors, N(ω)-nitro-L-arginine (10 mg/kg) or dexamethasone (0.5 mg/kg) attenuated the increase in NADPH-diaphorase activity. Glial fibrillary acidic protein (GFAP) was similarly induced 2 weeks after vagotomy in the vagal complex and surrounding area. Histamine H3 receptors in the vagal complex were visualized with [3H]N(α)-methylhistamine. The ligand-labeled H3 receptors were mainly located at the nucleus of the solitary tract (NST). The densities of H3 receptors did not change in the NST after unilateral vagotomy. These results suggest that peripheral axotomy such as mid-cervical vagotomy preferentially induces NOS in damaged neurons without affecting the level of H3 receptors.
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience