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Journal of Neuroscience, Vol 8, 2234-2247, Copyright © 1988 by Society for Neuroscience

ARTICLE

Effect of neonatal infraorbital nerve transection on substance P- and leucine enkephalin-like immunoreactivities in trigeminal subnucleus caudalis of the rat

RW Rhoades, NL Chiaia, PR Hess and MW Miller
Department of Anatomy, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine, Piscataway 08854.

The distributions of substance P-like immunoreactivity (SPLI) and leucine-enkephalin-like immunoreactivity (LENKLI) in subnucleus caudalis of normal adult rats were compared with those observed in the adult rats that sustained transection of the infraorbital (IO) nerve either on the day of birth or in adulthood. All immunocytochemical experiments in the neonatally nerve damaged rats were carried out at least 60 d after the nerve transection. In the animals that sustained nerve transections as adults, brains were processed for immunohistochemistry between 7 and 60 d after the lesions. In the rats that sustained IO nerve transections as adults, there was a transient reduction in the density of the SPLI in layers I and II of ipsilateral subnucleus caudalis. It was most apparent about 2 weeks after the nerve transection and returned to near normal values by 60 d after the lesion. In the rats that sustained IO nerve transections on the day of birth, there was no reduction in the density of SPLI in caudalis, and the band of staining on the deafferented side of the brain stem was actually 40% wider than that on the intact side. Neither neonatal nor adult IO nerve transection had appreciable effects upon the distribution of LENKLI in the rat's trigeminal brain-stem complex. In another series of experiments, rats that sustained neonatal transection of the IO nerve had this same nerve recut in adulthood. Twelve days after the second lesion, the brains of these animals were processed for SPLI. There was a marked reduction in the density of the staining for this peptide on the deafferented side. This last result is consistent with the interpretation that the increased distribution of SPLI in the neonatally nerve damaged rats is due, at least partially, to reorganization of primary afferents.

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