Effects of unilateral vagotomy on nitric oxide synthase and histamine H₃ receptors in the rat dorsal vagal complex

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.