The Anti-Inflammatory Agent Bindarit Attenuates the Impairment of Neural Development through Suppression of Microglial Activation in a Neonatal Hydrocephalus Mouse Model

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Figure 8.
Figure 8.

Altered morphology of cortical interneurons in prh mutants is partially rescued by bindarit treatment. A, The number of DLX5, a transcriptional factor which regulates parvalbumin-expressing cortical interneuron development, as an average in three ROIs shows no difference in DLX5-expressing interneurons among groups (two-way ANOVA followed by Tukey's test, n = 4 in each group; scale bars: 20 μm). B, The number of Calretinin+ (CALR+) interneurons as an average of three ROIs in upper layers is not significantly different among groups (left graph), but the percentages of CALR+ cells with processes is significantly reduced in veh-prh (†p = 0.0347 vs veh-WT, ‡‡p = 0.0086 vs bin-WT) and improved in bin-prh cortex (*p = 0.0299 vs veh-prh; right graph; two-way ANOVA followed by Tukey's test, n = 4 in each group; scale bars: 50 μm). C, The number of Calbindin D28K+ (CALB+) interneurons as an average of three ROIs in lower layers is not significantly different among groups (left graph), but the percentages of CALB+ cells with processes is significantly reduced in veh-prh (††p = 0.0025 veh-prh vs veh-WT, ††p = 0.0058 bin-prh vs veh-WT, ‡p = 0.0380 vs bin-WT) with no significant improvement in bin-prh cortex (p = 0.5564 vs veh-prh; right graph; two-way ANOVA followed by Tukey's test, n = 4 in each group; scale bars: 50 μm).

  1. The Journal of Neuroscience vol. 42 no. 9 1820-1844
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