Skip to main content
Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: C3aR signaling and gliosis in response to neurodevelopmental damage in the cerebellum

Fig. 6

Loss of C3aR in the Smarca5 cKO cerebellum results in increased apoptosis in the EGL and an early invasion of phagocyte cells. P1 (a) and P10 (b) cerebellums from control and mutant mice showing granule neuron precursors (Pax6+) in the EGL and NeuN+ granule neurons. At P10, the loss of Pax6+ cells from the EGL was observed in both the Smarca5 cKO and dKO cerebellum, and NeuN+ cells in the IGL were sparse in these mutants in comparison to control and C3aR KO cerebellums. Within the EGL of Smarca5 cKO and dKO mutant mice, cleaved caspase 3+ (cCasp3) apoptotic cells and TUNEL+ cells (arrows) were found in every section examined (c). These cCasp3+ cells in the EGL were occasionally observed within Iba1+ phagocyte cells (left-hand panel). d Iba1+ phagocytes were also observed in the EGL of Smarca5 cKO and dKO mutants at P10, though cCasp3+ cells were infrequent at this age. Most cCasp3+ cells observed at P10 were in the IGL (arrow, right-hand panel). The number of cCasp3+ and TUNEL+ cells (e) was highest in the dKO mice (n = 5 mice/genotype; error bars indicate standard error). However, only P1 dKO cerebellums showed a consistent, statistically significant increase in TUNEL labeling and cCasp3+ cells compared to Smarca5 cKO single mutants. At P10, TUNEL labeling was more variable; only the dKO cerebellums showed a statistically significant increase in TUNEL+ cells relative to the non-mutant control group at this age. Both the Smarca5 cKO and dKO cerebellums had high numbers of phagocytes in the EGL at P10 (f), whereas the Smarca5 cKO mutants had less than half as many as the dKO at P1 (n = 4 mice/genotype at each age; error bars indicate the standard error). *p < 0.05, **p < 0.005, ***p < 0.001 in e, f. Scale bars = 100 μm in all image panels

Back to article page