Research Paper Volume 7, Issue 9 pp 673—689

Figure 5. Microglial caspase-8 deficiency ameliorates MPTP-induced proinflammatory microglia activation in the striatum. Panel (a) shows illustration of Iba1 and CD16/32-labeled microglia in the striatum in response to either saline or MPTP in Casp8^fl/fl mice and Cre^LysMCasp8^fl/fl mice. Injection of saline in Casp8^fl/fl mice was not different from Cre^LysMCasp8^fl/fl mice and hence only Casp8^fl/fl mice saline is shown. Panels (b) and (c) show the stereological analysis of Iba1 (b) and CD16/32 (c) in the striatum in response to MPTP. Results are the mean ± SD of a minimum of four independent experiments and are expressed as number of cells per mm³. Statistical significance was calculated by analysis of variance followed by the least significant difference post hoc test for multiple range comparisons (p <0.05). Panel (d) shows illustration of dual immunofluorescence of Iba1 and CD16/32-labeled microglia in the striatum in response to either saline or MPTP in Casp8^fl/fl mice and Cre^LysMCasp8^fl/fl mice. Panel (e) show higher magnification photographs of dot boxes depicted in panel (d). Note the drastic changes in the microglia population in terms of Iba1-labeling in response to MPTP in both Casp8^fl/fl mice and Cre^LysMCasp8^fl/fl mice (a,d). Note the low levels of CD16/32 labeling in the unlesioned striatum (a, c, d) and how this marker is robustly up-regulated in response to MPTP in Casp8^fl/fl mice (a, c, d). Also note how the MPTP-induced up-regulation of proinflammatory microglia in tems of CD16/32 is hindered in Cre^LysMCasp8^fl/fl mice. Scale bar: a: 125 μm; d: Iba1 and CD16/32 staining: 50 μm; merge: 20 μm.