Research Paper Volume 13, Issue 16 pp 20319—20334

Inhibition of endoplasmic reticulum stress reverses synaptic plasticity deficits in striatum of DYT1 dystonia mice

Abnormal eIF2α signaling and ER stress in Tor1a+/- mice. (A) Ingenuity pathway analysis (IPA) was completed to identify significantly dysregulated canonical pathways. The top 15 pathways generated with the DEGs. (B) Gene Set Enrichment Analysis (GSEA) was applied to further confirm the up-regulated eIF2α signaling in Tor1a+/- mice. (C) Levels of mRNA in striatal lysates were measured by RT-qPCR. (D, E) Representative western blots of striatal lysates (D). Quantification of protein expression in striatum as shown (n: 3 per group). Data are represented as mean ±SEM. In each group, five mice were used (N=5), and three independent experiments were conducted for each mouse (n=3). P

Figure 3. Abnormal eIF2α signaling and ER stress in Tor1a+/- mice. (A) Ingenuity pathway analysis (IPA) was completed to identify significantly dysregulated canonical pathways. The top 15 pathways generated with the DEGs. (B) Gene Set Enrichment Analysis (GSEA) was applied to further confirm the up-regulated eIF2α signaling in Tor1a+/- mice. (C) Levels of mRNA in striatal lysates were measured by RT-qPCR. (D, E) Representative western blots of striatal lysates (D). Quantification of protein expression in striatum as shown (n: 3 per group). Data are represented as mean ±SEM. In each group, five mice were used (N=5), and three independent experiments were conducted for each mouse (n=3). P<0.05 was considered to be statistically significant.