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. Author manuscript; available in PMC: 2007 Nov 5.
Published in final edited form as: Brain Behav Immun. 2007 Feb 9;21(5):581–591. doi: 10.1016/j.bbi.2006.12.003

Table 1. Percentage of cells responding to SDF1 application.

We used calcium imaging to monitor the change in [Ca2+]i after chemokines are applied to acutely dissociated DRG from rats treated with vehicle or ddC. In all experiments, SDF1 and MCP1 were applied to the cells, followed by capsaicin, high K+ and ATP to characterize the cells. The number of cells responding to SDF1 application increased significantly by 14 days after ddC treatment. The number of cells responding to MCP1 application did not change in all experiments, suggesting CCR2 signaling is not part of the pain mechanism. Analysis of the cells responding to SDF1 application at PID7 and 14 revealed that most were non-neuronal based on their lack of response to capsaicin and high K+.

Table 1A. Percentage of neurons responding after chemokine application

Table 1B. Identity of cells responding to chemokine application

Condition SDF1 responsive neurons MCP-1 responsive neurons
Control - Saline injected (n=61) 4.9% (n=3) 4.9% (n=3)
ddC injection - PID 7 days (n=74) 16.2% * (n=12) 4.1% (n=3)
ddC injection - PID 14 days (n=58) 36.2% * (n=21) 3.4% (n=2)
Cell type PID7 PID14
SDF1 responsive neurons 16.2% (n=12) 36.2% (n=21)
Non-neuronal cells 83.3% (n=62) 63.8% (n=37)
*

p<0.01