Short- and long-term transganglionic changes in the central terminations of transected vibrissal afferents in the rat.

Previous light and electron microscopic studies in rat and cat have shown that transection of peripheral sensory nerve branches leads to alterations in the central branches of primary sensory neurons, so-called transganglionic changes. In this study the changes in choleragenoid (B)-horseradish peroxidase B-HRP-labeled primary sensory terminals and axons in the trigeminal nuclear complex 3-90 days following transection of vibrissae nerves in the rat have been studied. Since regeneration of the transected vibrissa nerve was not prevented, these experiments allowed the examination of degenerative changes in the earlier stage after nerve injury as well as those present during nerve regeneration and target reinnervation. Two different experimental approaches were used, depending on the postlesion survival time. For short-term experiments the deep vibrissa nerve was injected with a solution of B-HRP. Forty-eight hours later the nerve was transected at its entry in the follicle, and after survival times ranging from 3 to 15 days sections from the subnucleus caudalis and spinal trigeminal nucleus, were prepared for electron microscopic examination. For long-term experiments involving a 16- to 90-day posttransection survival time, the deep vibrissa nerve was cut first. Then B-HRP was injected into the reinnervated follicle 2 days before killing the rats. Atypical HRP-labeled terminals were seen from 4 to 90 days survival time. The changes observed included atypical swollen vesicles or lack of vesicles in parts of the terminals apposed to the synaptic cleft. Other terminals displayed dense clusters of vesicles, flocculent cytoplasm, and/or neurofilamentous hyperplasia. No evidence of complete disintegration or phagocytosis by glial cells was observed. From 4 to 12 days survival time the changes were most commonly seen in the larger terminals, from 19-90 days in smaller terminals. From 10 days survival time and onward, changes in axons were observed. The most commonly seen alterations were axons with expanded myelin sheaths. Normal-labeled terminals were seen at all survival times examined. Compared with earlier studies of transganglionic changes in the vibrissa system occurring after infraorbital nerve or vibrissa row nerve injury, the changes seen in this study are less pronounced. These observations indicate (1) that the initial changes in the central processes of peripherally injured vibrissae nerves are less extensive than those occurring after infraorbital nerve transection, possibly because of the distally located lesion, and (2) that transganglionic changes occur also after the injured nerve has regenerated.