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. Author manuscript; available in PMC: 2009 Aug 26.
Published in final edited form as: Neuroscience. 2008 Jun 19;155(3):948–958. doi: 10.1016/j.neuroscience.2008.06.024

Figure 3.

Figure 3

CFA-induced activation of PKCγ and its phosphorylation in the SCDH are attenuated in NR1 KO (Cre) mice at 1h and 48 h after CFA treatments. Confocal images of lumbar SCDH sections show the expression of PKCγ (red) and NeuN (green) 10 min after intraplantar saline (A) or CFA (B) Bar = 50 μm. PKCγ expression was detected in the inner layer of lamina II (arrowheads) while neuronal PKCγ expression is show as yellow labeling (arrows). (C) Immunoblots of lumbar SCDH samples at 10 min after the injection of intraplantar saline or CFA into the right (R) paw of NR1 floxed mice show increased expression of pPKCγ and PKCγ ipsilateral to the CFA injected paw. (D) Immunoblots of samples of the right lumbar SCDH collected at 10 min after the injection of intraplantar saline (S) or CFA into the right paw of GFP or Cre mice show decreased expression of pPKCγ and PKCγ in the SCDH of Cre mice. Actin immunoblots serve as loading controls. (E) Densitometric analysis of pPKCγ immunoblots. The data were normalized to saline treated GFP mice. The CFA induced expression of pPKCγ in lumbar SCDH is significantly reduced at 10 min and 48 h after intraplantar CFA in Cre compared to GFP mice. Data are the mean ± SEM (n = 3) (* p< 0.05).

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