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. 2017 Jul 14;4(4):ENEURO.0025-17.2017. doi: 10.1523/ENEURO.0025-17.2017

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Copyright © 2017 Briggs et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 3. — ER stress-related dysfunction is not observed in the APP^Swe model in vitro despite evidence of ISRIB target engagement. A, Thapsigargin-induced ER stress is not mitigated by ISRIB in APP^Swe mouse PCNs. Cells from nTg and Tg mice cultured for 13 DIV treated with 1 μM thapsigargin or 1 μM thapsigargin + 200 nM ISRIB have increased levels of ATF4 compared to vehicle control. nTg vehicle, n = 3; nTg + 1 μM thapsigargin, n = 3; nTg + 1 μM thapsigargin + 200 nM ISRIB, n = 3; Tg vehicle, n = 3; Tg + 1 μM thapsigargin, n = 3; Tg + 1 μM thapsigargin + 200 nM ISRIB, n = 3. B, Thapsigargin (1 μM) attenuates protein synthesis in nTg PCNs cultured for 7 DIV. ISRIB (200 nM) provides partial restoration of protein synthesis in PCNs challenged with thapsigargin. nTg vehicle + 10 μg/ml puromycin, n = 4; nTg + 1 μM thapsigargin + 10 μg/ml puromycin, n = 5; nTg + 1 μM thapsigargin + 200 nM ISRIB, n = 5. C, Thapsigargin-induced ER stress is not mitigated by ISRIB in nTg mouse PCNs. Cells from nTg mice cultured for 7 DIV treated with 1 μM thapsigargin or 1 μM thapsigargin + 200 nM ISRIB have increased levels of ATF4 compared to vehicle control. nTg vehicle, n = 6; nTg + 1 μM thapsigargin, n = 6; nTg + 1 μM thapsigargin + 200 nM ISRIB, n = 6. Error bars indicate SEM; **p < 0.01, *** p = 0.001, ****p < 0.0001.