Distribution, origin and plasticity of galanin-immunoreactivity in the rat carotid body

The distribution, origin and plasticity of galanin immunoreactivity in the rat carotid body was examined using an indirect immunofluorescence method. Galanin-immunoreactive nerve fibers were observed around the blood vessels as well as around the clusters of glomus and sustentacular cells. A double-immunofluorescence method revealed the coexistence of galanin- and calcitonin gene-related peptide-immunoreactivities in these nerve fibers. In the jugular, petrosal and nodose ganglia which supply the sensory nerve fibers to the carotid body, subpopulations of neurons showed both galanin- and calcitonin gene-related peptide-immunoreactivities. In the superior cervical ganglion, a few neurons were immunoreactive for galanin but not calcitonin gene-related peptide. While the nerve fibers showing both galanin- and calcitonin gene-related peptide-immunoreactivities disappeared after transection of the carotid sinus nerve, many galanin-immunoreactive nerve fibers without calcitonin gene-related peptide-immunoreactivity appeared throughout the operated carotid body. In addition, galanin-immunoreactive glomus cells which were not observed in the normal carotid body, were apparent at one and three days after transection of the carotid sinus nerve. At seven days after the carotid sinus nerve transection, the galanin-immunoreactive glomus cells disappeared. In the superior cervical ganglion, the number of galanin-immunoreactive neurons increased from one day after transection of the carotid sinus nerve. Within three days after the carotid sinus nerve transection in combination with superior cervical ganglion-ectomy, all galanin-immunoreactive nerve fibers disappeared, while many galanin-immunoreactive glomus cells appeared in the operated carotid body. At seven days after this operation, the number of galanin-immunoreactive glomus cells decreased and a few galanin-immunoreactive nerve fibers with or without calcitonin gene-related peptide-immunoreactivities appeared. Transection of the vagus nerve had no effect on the number or distribution of galanin-immunoreactivity in the carotid body. Disappearance of galanin- and calcitonin gene-related peptide-immunoreactive nerve fibers after transection of the carotid sinus nerve suggests that the majority of those nerve fibers originate from petrosal neurons which colocalize galanin- and calcitonin gene-related peptide-immunoreactivity. In addition, the carotid sinus nerve transection may cause the acquisition of galanin-immunoreactivity in originally immunonegative glomus cells, and in nerve fibers which probably originate from the superior cervical ganglion.