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. 2001 Sep 15;15(18):2421–2432. doi: 10.1101/gad.922801

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Copyright © 2001, Cold Spring Harbor Laboratory Press

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JIP1 deficiency causes increased survival of hippocampal neurons following exposure to excitotoxic stress in vitro. Hippocampal neurons were cultured in vitro (11 d) and treated without and with kainic acid (100 μM; 30 min). Cell survival after 24 h was examined by immunocytochemistry by staining neurons with an antibody to MAP-2. Representative microphotographs of unchallenged wild-type (A), Jip1^−/− (C), and Jnk3^−/− (E) neurons are presented. The effect of kainate treatment on wild-type (B), Jip1^−/− (D), and Jnk3^−/− (F) neurons is shown. The scale bar represents 50 μm. (G) Cell survival in three independent experiments was quantitated (mean ± SD).

JIP1 deficiency causes increased survival of hippocampal neurons following exposure to excitotoxic stress in vitro. Hippocampal neurons were cultured in vitro (11 d) and treated without and with kainic acid (100 μM; 30 min). Cell survival after 24 h was examined by immunocytochemistry by staining neurons with an antibody to MAP-2. Representative microphotographs of unchallenged wild-type (A), Jip1^−/− (C), and Jnk3^−/− (E) neurons are presented. The effect of kainate treatment on wild-type (B), Jip1^−/− (D), and Jnk3^−/− (F) neurons is shown. The scale bar represents 50 μm. (G) Cell survival in three independent experiments was quantitated (mean ± SD).

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