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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Neuropharmacology. 2015 May 13;99:242–255. doi: 10.1016/j.neuropharm.2015.04.034

Figure 5.

Figure 5

CB1R and mGluR2/3 expression is reduced in WIN55-treated female mice. (A-D)

Single optical section images were acquired at 40x magnification and a 1.5x Zoom from cortical layer 5 of the PL mPFC, top panels show images from control mice, middle panels show images from WIN55-treated mice (scale bar = 50 µm) and lower panels give mean intensity of control (open bars) and WIN55-treated (filled bars) groups. (A) Mean intensity of the CB1R fluorescent signal in layer 5 of the PL mPFC of WIN55-treated mice was not significantly different from control mice (p=0.0576). (B) Mean intensity of mGluR2/3 signal in WIN55-treated mice showed a modest decrease in the mPFC (~35%, p = 0.0417). Mean intensity of MAGL (C) and VGluT1 (D) staining in WIN55-treated mice were not different from those found in control animals (p > 0.05). (E) Single optical section images were acquired at 40x magnification and a 7x Zoom from cortical layer 5 of the PL mPFC. The first column (left) in green shows CB1R labeling, second column (middle) in red shows VGluT1, and column 3 (right) shows the merged signals. Top panels show images from control mice and lower panels show images from WIN55-treated mice (scale bar = 10 µm). WIN55-treated animals showed a modest decrease in CB1R co-localized with vGlut1 in L5 in the PL mPFC (~40%, p = 0.0351). White arrows indicate examples of CB1R co-localized with VGluT1.