Long-term age-related consequences of forelimb damage upon expression of primary afferent phenotypes in the cervical dorsal horn.

Abstract

Rats that sustained forelimb removal on either embryonic day 16 (E-16) or the day of birth (P-0), or transection of the brachial plexus in adulthood, had sections through the cervical dorsal horn stained for galanin, calcitonin gene-related peptide (CGRP), or the plant lectin Bandieria simplicifolia-I (BS-I) 35-50 days after these lesions. The results of these experiments demonstrated age-related differences in the effects of peripheral nerve damage upon the distributions of each of these three primary afferent markers in the dorsal horn. Damage to the brachial plexus in adulthood caused a significant increase in the density of galanin immunoreactivity in the medial portion of layers I and II and the appearance of galanin immunoreactivity in layers III and IV of the cervical dorsal horn. Such lesions resulted in significant reductions in the density of CGRP immunoreactivity in layers I and II and of BS-I binding in lamina II. Forelimb removal on the day of birth resulted in no significant change in the density of galanin immunoreactivity in layers I and II, but in the appearance of galanin-immunoreactive fibers in layers III-V. Neonatal forelimb removal resulted in no significant change in the density of CGRP immunoreactivity in layers I and II, but in a significant reduction in the density of BS-I binding in the medial portion of lamina II. Removal of the forelimb on E-16 caused a significant increase in the density of galanin immunoreactivity in layers III-V, but had no significant effect on the density or distribution of either CGRP immunoreactivity or BS-I binding in the cervical dorsal horn. These results suggest that peripheral nerve damage at all ages may cause an up-regulation of galanin in a wider distribution of ganglion cell types than was previously thought to be the case, and that there are different sensitive periods for lesion-induced, long-term changes in the innervation of the dorsal horn by CGRP- and BS-I-positive primary afferent axons.