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Introduction: Neuropathic pain is a common, debilitating occurrence after spinal cord injury (SCI). EphB signaling has been implicated in neuropathic pain, but different populations of neurons that upregulate EphB after SCI must be discovered. Understanding whether EphB2 is upregulated in specific subpopulations of dorsal horn interneurons (e.g. those expressing PKCgamma or calretinin) after injury would increase the understanding of SCI-induced neuropathic pain.

Methods: Mice were either given a contusion-type SCI (n=7) or a laminectomy-only (n=6) at cervical level 5/6. After two weeks of recovery, mRNA was labeled using RNAscope in the sectioned spinal cords. Four different targets were visualized in the sections via confocal microscopy: nuclei, PKCgamma mRNA, calretinin mRNA, and EphB2 mRNA.

Results: An average of 6.15 EphB2 mRNA transcripts were visible per PKCgamma positive interneuron in mice with SCI compared to an average of 5.38 in the laminectomy-only controls. These results were not significantly different using a Student’s t-test (p-value = 0.28). As for calretinin expressing interneurons, an average of 5.15 EphB2 transcripts were present in mice with SCI while an average of 4.83 transcripts were present in the laminectomy-only control group. Again, these results were not significantly different (p-value = 0.24).

Discussion: Given our results, it is unlikely that an increase in EphB2 expression in PKCgamma or calretinin expressing interneurons is involved in the development of neuropathic pain after SCI. To find mechanisms underlying SCI-induced neuropathic pain, future studies could examine EphB2 upregulation in different populations of interneurons.