Research Paper Volume 7, Issue 9 pp 673—689

Figure 4. Microglial caspase-8 deficiency ameliorates proinflammatory microglia activation in the substantia nigra in response to MPTP.

Panel (a) shows an illustration of Iba1 and CD16/32-labeled microglia in the substantia nigra 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. Inserts are high-magnification photographs to show more precisely the morphological features of microglia. Panels (b) and (c) show the stereological analysis of total microglia (Iba1) (b) or proinflammatory microglia (CD16/32) (c) in the substantia nigra of Casp8^fl/fl mice and Cre^LysMCasp8^fl/fl mice after 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 substantia nigra in response to saline or MPTP in Casp8^fl/fl mice and Cre^LysMCasp8^fl/fl mice. Panel (e) are higher magnification photographs of dot boxes depicted in Note the drastic changes in the microglia morphology in terms of Iba1-labeling in response to MPTP in both Casp8^fl/fl mice and Cre^LysMCasp8^fl/fl mice (a, d). Also note how CD16/32-immunolabeled proinflammatory microglia is strongly up-regulated in response to MPTP in Casp8^fl/fl mice, particularly in the pars compacta of SN (a,d), this effect being notably hindered in Cre^LysMCasp8^fl/fl mice. Scale bar: a: 350 μm; d: Iba1 and CD16/32 staining: 300 μm; merge: 35 μm.