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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: Hippocampus. 2011 Jan;21(1):81–92. doi: 10.1002/hipo.20725

Figure 2. Localization of phosphacan and RPTPβ in deafferented dentate gyrus 2 and 7d after UEC.

Figure 2

Projected z stack images show phosphacan (3F8) signal at 2d (A, B) shows predominant localization over the granule cell body layer (GCL) and subgranular zone (SGZ) of contralateral control (arrows in A). After lesion (B), phosphacan is increased in the outer molecular layer (OML, arrows) and decreased in the GCL and SGZ. By contrast, the distribution of RPTPβ at 7d post-lesion (C, D) is punctate and visible throughout the ML at higher density (D) than in the contralateral control (C). Confocal dual labeling of phosphacan at 2d (green in E) and RPTPβ at 7d (green in F) with astrocyte marker (GFAP, red) in the deafferented ML suggests that reactive astrocytes are not the principal source of either splice variant. The two markers fail to show significant overlap of signal (white arrows in panels E,F). Individual examples of reactive astrocytes (yellow arrows) are show enlarged in each inset. Minus primary controls had only low background signal (G). Bar in A–D=20µm; E–G=40µm; insets=5 µm.