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. Author manuscript; available in PMC: 2015 Jan 29.
Published in final edited form as: J Neuroimmunol. 2006 Jul 10;178(0):9–16. doi: 10.1016/j.jneuroim.2006.05.027

Fig. 1.

Fig. 1

CCL2, μ-opioid receptor (MOR), and CCR2 immunocytochemical co-localization with glial fibrillary acidic protein (GFAP) in subpopulations of striatal astrocytes in wild type (A,B,D–F) and CCR2(−/−) mice (C,G–I). A small subpopulation of astrocytes normally express MOR (arrows in A), CCL2 (arrow in B), or CCR immunoreactivity (arrows in F), although the proportion possessing MOR (A) (El-Hage et al., 2006), or CCL2 (B), immunoreactivity increases following morphine and/or Tat exposure (see Fig. 2A) (scale bar A–B, = 25 μm; C = 15 μm). MOR could be localized in a subset of astrocytes in CCR2−/− mice (arrowheads in C delineate astrocytes with highly polarized MOR and GFAP cytoplasmic immunofluorescence; Hoechst counterstained nuclei). CCR2 immunoreactivity was present in wild type (D–F; arrows in F), but not in CCR2 (−/−) null (G–I) mice (D–I; scale bar = 20 μm).