FIGURE 9.

Increased unfolded protein response pathway is associated with earlier astrocyte activation. (a) Western blot analyses of age‐matched uninfected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brains for unfolded protein response components as indicated, β‐Actin displayed as a loading control. (b) Quantitation of relative expression levels of eIF2α in uninfected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brains. Not significantly different, Student's t‐test. (c) Quantitation of relative expression levels of PERK uninfected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brain. Not significantly different, Student's t‐test. (d) Western blot analysis of 98 dpi prion‐infected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brain for unfolded protein response components as indicated. (e) Quantitation of the percentage of total phosphorylated eIF2α in 98 dpi prion‐infected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brain. *P < .05, Student's t‐test. (f) Quantitation of the percentage of total phosphorylated PERK in 98 dpi prion‐infected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brain. *P < .05, Student's t‐test. (g) Immunohistochemical analysis of phosphorylated PERK (PERK‐P; red) and GFAP (green) in 98 dpi prion infected, terminal prion infected and age‐matched uninfected Csf1r ^WT and Cs1fr ^ΔFIRE superior colliculus (G3). Scale bars = 100 μm or 20 μm as indicated. (h) Western blot analysis of terminal prion‐infected brain homogenates probed for unfolded protein response components as indicated, β‐Actin displayed as a loading control. (i) Quantitation of the percentage of total phosphorylated eIF2α in terminal prion‐infected Csf1r ^WT and Cs1fr ^ΔFIRE mouse brains. Not significantly different, Student's t‐test. Points show individual mice. Panels A‐G, N = 4 mice/group. Horizontal bar = median. Panels H&I, N = 5–6 mice/group