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. 2015 Mar 3;24(11):3257–3271. doi: 10.1093/hmg/ddv080

Figure 6.

Figure 6.

In the absence of BDNF-TrkBR signaling, the HD iPSC-derived striatal-like neural progenitors die due to glutamate toxicity. (A) Acute BDNF withdrawal in the HD iPSC-derived cultures (grey and black) up-regulated the GRIN2B subunit of the NMDA receptor (*P < 0.05, Student's t-test). (B) The cell death phenotype in the HD cultures (grey and black) is reversed using memantine, a small molecule blocker of NMDARs (*P < 0.05, **P < 0.001, ***P < 0.0001; one-way ANOVA). (C) The cell death phenotype in the HD cultures (grey and black) is reversed using SB23906, a small molecule blocker of cleaved p38 (*P < 0.05, **P < 0.001, ***P < 0.0001; one-way ANOVA). (D) The cell death phenotype in the HD cultures (grey and black) is reversed using CNQX, a small molecule blocker of the AMPA/Kainate receptors (*P < 0.05, **P < 0.001, ***P < 0.0001; one-way ANOVA). (E) The cell death phenotype in the HD cultures (grey and black) is reversed using s-MCPG, a small molecule blocker of group I/II mGluRs (*P < 0.05, **P < 0.001, ***P < 0.0001; one-way ANOVA). (F) The cell death phenotype in the HD cultures (grey and black) is reversed using BAPTA, a small molecule blocker of calcium influx (*P < 0.05, **P < 0.001, ***P < 0.0001; one-way ANOVA).