<p><b>Copyright information:</b></p><p>Taken from "Delayed functional expression of neuronal chemokine receptors following focal nerve demyelination in the rat: a mechanism for the development of chronic sensitization of peripheral nociceptors"</p><p>http://www.molecularpain.com/content/3/1/38</p><p>Molecular Pain 2007;3():38-38.</p><p>Published online 12 Dec 2007</p><p>PMCID:PMC2228278.</p><p></p> MCP-1 expression was increased by LPC-induced nerve injury within the IB-labeled neuronal group in both the DRG ipsilateral and contralateral to the nerve injury. Sham-injury treatment did not produce significant changes in the extent of MCP-1/IBcolocalization. CCR2 expression was increased by LPC-induced nerve injury within IB-labeled neuronal group in both the DRG ipsilateral and contralateral to the nerve injury. Like, MCP-1, sham-injury treatment did not produce significant changes in CCR2/IB4 colocalization in either DRG ipsi- or contralateral to the sham injury. IP-10 expression was increased by LPC-induced nerve injury within IB-labelled neuronal group in both the DRG ipsilateral and contralateral to the nerve injury, while sham-injury treatment did not produce significant changes in IP-10/IBcolocalization. Comparisons of immunoreactive cell percentages were made between LPC-treatment and sham-treated animals. Data represent means ± SE. Analysis was performed using two-way ANOVA followed by the Bonferroni post-hoc pair-wise comparisons (*p < 0.01)
