COLLATERAL SPROUTING OF UNINJURED PRIMARY AFFERENT A-FIBERS INTO THE SUPERFICIAL DORSAL HORN OF THE ADULT-RAT SPINAL-CORD AFTER TOPICAL CAPSAICIN TREATMENT TO THE SCIATIC-NERVE

That terminals of uninjured primary sensory neurons terminating in the dorsal horn of the spinal cord can collaterally sprout was first sugg ested by Liu and Chambers (1958), but this has since been disputed. Re cently, horseradish peroxidase conjugated to the B subunit of cholera toxin (B-HRP) and intracellular HRP injections have shown that sciatic nerve section or crush produces a long-lasting rearrangement in the o rganization of primary afferent central terminals, with A-fibers sprou ting into lamina II, a region that normally receives only C-fiber inpu t (Woolf et al., 1992). The mechanism of this A-fiber sprouting has be en thought to involve injury-induced C-fiber transganglionic degenerat ion combined with myelinated A-fibers being conditioned into a regener ative growth state. In this study, we ask whether C-fiber degeneration and A-fiber conditioning are both necessary for the sprouting of A-fi bers into lamina II. Local application of the C-fiber-specific neuroto xin capsaicin to the sciatic nerve has previously been shown to result in C-fiber damage and degenerative atrophy in lamina II. We have used B-HRP to transganglionically label A-fiber central terminals and have shown that 2 weeks after topical capsaicin treatment to the sciatic n erve, the pattern of B-HRP staining in the dorsal horn is indistinguis hable from that seen after axotomy, with lamina II displaying novel st aining in the identical region containing capsaicin-treated C-fiber ce ntral terminals. These results suggest that after C-fiber injury, unin jured A-fiber central terminals can collaterally sprout into lamina II of the dorsal horn. This phenomenon may help to explain the pain asso ciated with C-fiber neuropathy.