REORGANIZATION OF CENTRAL TERMINALS OF MYELINATED PRIMARY AFFERENTS IN THE RAT DORSAL HORN FOLLOWING PERIPHERAL AXOTOMY

We have investigated the time course and extent to which peripheral ne rve lesions cause a morphological reorganization of the central termin als of choleragenoid-horseradish peroxidase (B-HRP)-labelled primary a fferent fibers in the mammalian dorsal horn. Choleragenoid-horseradish peroxidase is retrogradely transported by myelinated (A) sensory axon s to laminae I, III, IV and V of the normal dorsal horn of the spinal cord, leaving lamina II unlabelled. We previously showed that peripher al axotomy results in the sprouting of numerous B-HRP-labelled large m yelinated sensory axons into lamina II. We show here that this spread of B-HRP-labelled axons into lamina II is detectable at 1 week, maxima l by 2 weeks and persists for over 6 months postlesion. By 9 months, h owever, B-HRP fibers no longer appear in lamina II, The sprouting into lamina II occurs whether regeneration is allowed (crush) or prevented (section with ligation), and does not reverse at times when periphera l fibers reinnervate the periphery. We also show that 15 times more sy naptic terminals in lamina II are labelled by B-HRP 2 weeks after axot omy than in the normal. We interpret this as indicating that the sprou ting fibers are making synaptic contacts with postsynaptic targets. Th is implies that A-fiber terminal reorganization is a prominent and lon g-lasting but not permanent feature of peripheral axotomy. We also pro vide evidence that this sprouting is the consequence of a combination of an atrophic loss of central synaptic terminals and the conditioning of the sensory neurons by peripheral axotomy. The sprouting of large sensory fibers into the spinal territory where postsynaptic targets us ually receive only small afferent fiber input may bear on the intracta ble touch-evoked pain that can follow nerve injury. (C) 1995 Wiley-Lis s, Inc.