Degeneration and regeneration of peripheral nerve in the rat trigeminal system. II. Response to nerve lesions

Authors


Abstract

The course of vibrissa sensory receptor denervation and subsequent reinnervation was studied following transection or crush of the rat infraorbital nerve. Eighteen hours after nerve lesion, the large-diameter myelinated nerves supplying the lanceolate receptors of the intermediary zone and the Merkel cells of the stratum basale contained areas of focal axoplasmic abnormalities, and some of the nerve terminals exhibited vacuolization, mitochondrial swelling, and disruption of the neurofilament pattern. The Merkel cells and lanceolate receptors of the intermediary zone were completely deafferented by 24 hours after the nerve injuries. The Ruffini complex, free nerve endings and lanceolate receptors of the inner conical body, as well as the free nerve endings and lanceolate receptors of the connective tissue below the Ringwulst, were completely normal 24 hours after crush or transection of the nerve. These receptors underwent progressive degeneration from days 2 through 6 and the vibrissa was totally denervated by day 7. Regenerating axons were first seen entering the vibrissae 2 weeks after the crush lesion and 1 month following nerve transection. Except for a slight decrease in the percentage of Merkel cells innervated, vibrissae from postcrush animals were virtually indistinguishable from normal by 3 months. In contrast, vibrissae from rats subjected to the transection lesion exhibited evidence of misdirected axons and abnormally reinnervated receptors throughout the course of regeneration. Axons entering the hairs with the main vibrissal nerve were observed contributing to the innervation of the inner conical body, an area normally supplied exclusively by the conus nerve. Many of the lanceolate receptors contained multiple unmyelinated axons, and the usually highly ordered circular innervation of the inner conical body was markedly abnormal. It is suggested that these results may help explain the faulty sensory localization and abnormal sensations reported by patients suffering a peripheral nerve injury.

Ancillary