Afferent innervation in dorsal horn at cervical level after spinal cord injury in rats

Cervical spinal cord injury (cSCI) damages spinal pathways, leading to major motor impairments. Although many studies have focused on reporting motor deficits following SCI, understanding how sensory neurons are altered by cSCI is an important aspect to promote recovery of function. Indeed, afferent activation may represent a potential driver of motor plasticity and recovery. Previous results from our lab have shown that activation phrenic afferents induce respiratory motor plasticity in both spinal intact animals and animals receiving a C2 hemisection injury (C2Hx). However, little is known about the impact of C2Hx on sensory afferent expression in the dorsal horn. Here we examined afferent expression in the dorsal horn of spinal segments associated with the phrenic motor nucleus (C3-C5) 8 weeks after C2Hx. Male and female Sprague-Dawley rats (n=9 each) either received a left hemisection at C2 and recovered for 8 weeks or served as age matched controls (n=5 male; n=4 female). Using immunohistochemistry we have begun examining CGRP (calcitonin gene related peptide), as a marker of medium size afferent fibers, and PV (parvalbumin), as a marker for large diameter proprioceptive fibers. We tested the hypothesis that expression of CGRP and PV following C2Hx would be increased in the dorsal horn compared to controls. When males and females are pooled, our preliminary data show no change in CGRP mean fluorescent pixel intensity normalized by area following C2Hx (73.13 ± 18.82; n=4) compared to controls (89.81 ± 16.12; n=4). Our PV results also show no statistical difference between SCI and controls (87.16 ± 12.00; n=4 vs 74.14 ± 4.82; n=4). In this ongoing project, we are also evaluating the expression of small diameter afferents with the marker isolectin B4 (IB4) and the results will be analyzed to examine if sex impacts afferent expression. Understanding how sensory afferents reorganize following cSCI is important to maximize respiratory motor plasticity and improve breathing after injury. This work was supported by funding from the NIH: R00 HL143207-01 (KAS), Craig H. Neilsen Grant 993667 (KAS), NCATS-NIH: 2TL1 TR001437 (TCH). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.