Skip to main content
Figure 3 | Molecular Pain

Figure 3

From: Expression of inwardly rectifying potassium channels by an inducible adenoviral vector reduced the neuronal hyperexcitability and hyperalgesia produced by chronic compression of the spinal ganglion

Figure 3

Behavioral effects of adenoviral vectors in CCD rats. At day 0, either the vehicle, the control vector (AdEGI), or the vector containing the Kir2.1 gene (AdKir) was delivered to the L4 DRG via sub-epineurial injection. The ganglion was then compressed (closed arrowhead). The inducing agent was delivered by IP injection (open arrow) either immediately (A) or after a delay of 3 days (B). In either case, the inducing agent was delivered again at postoperative day 10. Same format as Figure 2. Hyperalgesia (decreased mean foot withdrawal threshold, FWT) after CCD was obtained on the ipsilateral (Ipsi) but not contralateral (Con) foot. The magnitude of hyperalgesia produced by CCD (A,B, open squares, solid lines) was the same with or without the presence of the control virus (A, solid squares, dashed lines) and was greater than that produced by the control or AdKir viral vectors in the absence of CCD (Figure 2, open and closed squares). The increased hyperalgesia produced by CCD, in comparison with that produced by the viral vectors alone was significantly reduced by the induction of AdKir (A, solid squares, solid line) but only if the induction occurred at the time of compression and not if it occurred after a delay of 3 days (B). *: P < 0.05 vs. pre-operative mean for the ipsilateral foot of all groups in A-C; †: P < 0.05, AdKir vs. AdEGI or vehicle group for the ipsilateral foot (A).

Back to article page