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. 2015 Dec 16;41(6):1670–1680. doi: 10.1038/npp.2015.337

Figure 3.

Figure 3

Endoneuraminidase N (EndoN) attenuates some measures of neuroplasticity following fluoxetine (FLX) treatment and chronic unpredictable stress (CUS). (a) Mean+SEM density of PSA-NCAM-ir cells in the granule cell layer (GCL). EndoN reduced PSA-NCAM-ir cells in the dentate gyrus regardless of CUS or FLX (*p<0.0005). (b) Mean±SEM density of BrdU-ir cells in the GCL. EndoN and CUS reduced neurogenesis in the ventral GCL. However, FLX treatment reduced neurogenesis when given to the EndoN treated group (*p<0.04, #p<0.04). (c) Mean+SEM density of Ki67-ir cells in the GCL. FLX treatment increased cell proliferation (Ki67-ir cells) in the ventral region compared with VEH treatment, regardless of group (*p<0.04). (d) Mean+SEM density of cFos-ir cells in the GCL. Expression of cFos-ir cells was reduced in the CUS groups after acute swim stress (p<0.05), whereas under CUS EndoN reversed the FLX-induced decrease in cFos-ir cells (*p<0.03). (e–i) Photomicrographs of (e) PSA-NCAM in vehicle treated and (f) EndoN treated groups with a fluorescent secondary antibody and taken with a confocal microscope for improved clarity and contrast. Photomicrographs of (g) NeuN-ir cells in the GCL, (h) BrdU-ir cells in the GCL and (i) merged BrdU/NeuN-ir cell with confocal stacks in the x–z plane (j) and in the y–z plane (k). n=6–10 per group.