Figure 4.

Disruption of neural activity in the peri-lesional tissues surrounding microinfarcts. (a, b) Focal photothrombosis is targeted away from a penetrating arteriole (green; off-target) or directly atop a penetrating arteriole (red; on-target). C-Fos expression in response to whisker stimulation was examined 3, 8, and 20 days following microinfarct induction. Microinfarcts were strategically placed such that their peri-lesional region overlapped with the primary barrel cortex. (c) Example images of c-Fos staining in barrel cortex. The relative location of each image is shown in insets of panels (a) and (b) (black square, 800 × 800 µm area). (d) The number of c-Fos-positive cells decreased in peri-lesional tissues, with the greatest change in the acute time-frame of three days after occlusion (p = 0.002 main effect, F(1.97,3.93) = 135.6, one-way ANOVA with repeated measures; *p < 0.05, compared to 1000 µm bin with Tukey post hoc analysis). This decrease in c-Fos is not seen with off-target control irradiations (green). While gradual recovery of activity was observed, persistent deficits were detected eight days (p = 0.006 main effect, F(1.38, 2.76) = 59.73, one-way ANOVA with repeated measures) and 20 days after onset (p = 0.006 main effect, F(1.67, 3.34) = 34.56, one-way ANOVA with repeated measures). For all data, c-Fos-positive cell counts were normalized to the averaged cell counts obtained from the barrel cortex of three stimulated, but sham treated C57BL/6 mice (no Rose Bengal but laser irradiation). Data are mean ± SEM. Panels (d) to (f) comprise data from n = 3 mice (each with one penetrating arteriole occlusion) for each post-occlusion time-point and the off-target control. (e, f) No change in NeuN-positive cell number or VGlut2 intensity was detected in peri-lesional tissues. Data is mean ± SEM.