Skip to main content
Figure 3 | Molecular Pain

Figure 3

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

Figure 3

Percentage of MCP-1, CCR2 and IP-10 immunoreactive neurons with IB4-positive neuronal profiles on POD 14. MCP-1 expression was increased by LPC-induced nerve injury within the IB4-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/IB4 colocalization. CCR2 expression was increased by LPC-induced nerve injury within IB4-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 IB4-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/IB4 colocalization. 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).

Back to article page