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Spinal Cord Expression and Function of Complement C5aR1 Receptor in Neuropathic Pain
Abstract   Peer reviewed

Spinal Cord Expression and Function of Complement C5aR1 Receptor in Neuropathic Pain

Kiley Christopher, Alex Keyes, Kavita Solanki, Yaroslav Andrianov, L. Shutov, C Warwick, Trent Woodruff, P. Belan, N. Voitenko and Yuriy Usachev
The journal of pain, Vol.25(4 Supplement), pp.5-5
04/2024
DOI: 10.1016/j.jpain.2024.01.030

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Abstract

Chronic pain affects approximately 100 million Americans and only a minority of patients experience satisfactory relief of their pain with currently available pharmaceutics. One type of chronic pain is caused by direct injury to the nerve called neuropathic pain, which affects ~10% of the overall population. Despite the prevalence, the underlying mechanisms of neuropathic pain are not well-defined, and better understanding of the mechanisms that promote central sensitization after injury could lead to better treatment of this condition. Notably, a recent meta-analysis of microarray studies of pain-related genes demonstrated a remarkable enrichment of genes related to the complement system activation. Among the complement products, C5a and its receptor C5aR1 seem to be especially important in the pathogenesis of neuropathic pain. However, it is not well understood how C5a/C5aR1 signaling contributes to pain amplification in the spinal cord and which cells are involved. Here, we used immunohistochemistry (IHC) to examine which cells within the spinal cord express C5aR1. Our data show that C5aR1 is expressed primarily in microglia and astrocytes, but not in neurons. To further investigate the function of C5aR1, we have generated two mouse lines with C5aR1 deletion specifically in microglia and astrocytes, respectively to test the roles of C5aR1 in these cell types during neuropathic pain. Our data suggest that C5aR1 expressed in microglia is essential for the initiation of neuropathic pain. Collectively, these results provide a new mechanistic insight into the role of C5a/C5aR1 signaling in neuropathic pain. Research reported in this presentation is supported by the NIH/NIGMS grant T34GM141143 (K.C.), NIH/NINDS grant R01NS131189 (Y.M.U.), the University of Iowa (UI) Office of the Vice President for Research, Graduate College, College of Liberal Arts and Sciences, Department of Biology, and Office of the Provost (K.C.).

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