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Fig. 6 | Molecular Neurodegeneration

Fig. 6

From: CNS axonal degeneration and transport deficits at the optic nerve head precede structural and functional loss of retinal ganglion cells in a mouse model of glaucoma

Fig. 6

Sustained Dex-induced IOP elevation causes robust activation of astrocytes in ONH, ON and retina. Longitudinal sections of optic nerves (a) and whole mount retinas (b) were collected from 10 weeks post Veh or Dex-injected mice, and immunostained for reactive astrocytes with GFAP (green). a Hypertrophic reactive astrocytes with increased expression of GFAP were observed in ONH cross sections in 10 weeks Dex-injected mice (n = 5) compared to Veh-injected mice (n = 3). b Immunostaining of whole mount retinas with GFAP (green) and RBPMS (red) show relatively higher number reactive astrocytes and decreased RGCs in 10 weeks Dex-injected mice compared to Veh-injected mice (n = 8). c For comparisons, longitudinal sections of aged-matched human normal and glaucomatous optic nerves were immunostained with antibodies specific for GFAP and neurofilament-heavy chain (NF-H) (red). Loss of NF-H with increased GFAP expressing reactive astrocytes are observed throughout the length of human glaucomatous optic nerve compared to aged-matched normal human optic nerve. In addition, there is a robust activation of astrocytes in human glaucomatous ONH (n = 5) compared to normal ONH (n = 4)

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