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. Author manuscript; available in PMC: 2013 Nov 22.
Published in final edited form as: J Neurosci. 2013 Mar 27;33(13):10.1523/JNEUROSCI.3342-12.2013. doi: 10.1523/JNEUROSCI.3342-12.2013

Figure 9.

Figure 9

Sustained pain-related behavior in scLRP1−/− mice is associated with phosphorylation of p38 MAPK (P-p38MAPK) and activation of microglia in the spinal dorsal horn. (A–D) Immunofluorescence for P-p38MAPK in the spinal dorsal horn of mice in uninjured (A,B) and injured (C,D) seven days after PNL. (E,F) Immunofluorescence of cd11b/OX-42 in the spinal dorsal horn after seven days of PNL injury. Images are representative of those obtained in studies with 3–4 mice per cohort. Each pair of images shown in panels A-F (A and B, C and D, E and F) is matched for exposure. Scale bar, 400 µm (G, H) Quantification by densitometry of P-p38MAPK and OX-42 in the ipsilateral and contralateral spinal dorsal horn. Signal intensity in the ipsilateral horn was significantly increased in scLRP1−/− mice compared with scLRP1+/+ mice (*p<0.05, n=4/group). Signal intensity also was significantly increased in the ipsilateral compared with the contralateral horn for each biomarker (*p<0.05). (I) Immunoblot analysis of P-p38 MAPK in spinal cord dorsal horn isolated seven days after PNL. Equal amounts of protein (50 µg) were loaded in each lane and subjected to SDS-PAGE. Total p38 MAPK was determined as a loading control. (J) Quantification of P-p38MAPK to T-p38MAPK ratio by densitometry in uninjured and injured spinal cord (n=3–4 mice) *p<0.05 comparing injury in each genotype.