Regeneration of the recurrent laryngeal nerve in the guinea pig: reorganization of motoneurons after freezing injury.

The purpose of this study was to clarify the morphologic changes resulting from reinnervation after a freezing injury. We chose the freezing injury as the most promising nerve regeneration model in order to examine the mechanism behind the production of misdirected reinnervation. The left recurrent laryngeal nerve of the adult guinea pig was injured by freezing (-80 degrees C) at the level of the 10th tracheal ring. At intervals ranging from 2 weeks to 6 months after the injury, horseradish peroxidase was injected into the left posterior cricoarytenoid muscle to ascertain the presence of retrograde-labeled perikarya in the medulla oblongata. Projections to the individual laryngeal muscles and to the entire recurrent laryngeal nerve served as normal controls. In addition, we observed by electron microscopy the degeneration and regeneration processes of the recurrent laryngeal nerve following injury. From 2 to 6 months after the freezing injury, the number of labeled neurons in the nucleus ambiguus increased gradually from 20 to 90. In addition, the area occupied by neurons which project to the posterior cricoarytenoid muscle was expanded, but was confined within the region of perikarya projecting to the normal recurrent laryngeal nerve. Most axons degenerated within 3 days and showed regenerative sprouting with growth cones by 7 days postinjury. Despite the fact that freezing injury preserved the basal lamina tunnel with minimal disturbance of the recurrent laryngeal nerve fiber structure, target-specific reinnervation was incomplete.