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. 2022 Jun 8;7(11):e155002. doi: 10.1172/jci.insight.155002

Figure 3. Neurabin deficiency enhances A1R-mediated neuroprotective Akt signaling in neurons.

Figure 3

(A) PI3K/Akt signaling is required for A1R-mediated neuroprotection against glutamate excitotoxicity. WT hippocampal neurons (13–14 DIV) were treated under indicated conditions. Representative images of live (green) and dead (red) neurons are shown. (B) Quantitation of cell survival under indicated treatment. ***P < 0.001; ****P < 0.0001 by 1-way ANOVA multiple comparisons. Sample numbers are indicated in parentheses. (C) Neurabin deficiency enhances A1R-mediated Akt activation in neurons. Primary hippocampal neurons derived from WT or neurabin deficiency (Ppp1r9a–/–) mice were treated with R-PIA at the indicated concentrations. Representative Western blots are shown. (D) Quantitation of phospho-Akt (pAkt, Thr308). ***P < 0.001 by 2-way ANOVA. n = 4/group. (E) Neurabin deficiency prolongs the A1R-mediated Akt response in neurons. WT and Ppp1r9a–/– neurons were stimulated with 1 μM R-PIA for the indicated time durations. Representative blots are shown. (F) Quantitation of pAkt levels. *P < 0.05; **P < 0.01; ****P < 0.0001 by 2-way ANOVA multiple comparisons. n = 4/group. Data were shown as mean ± SEM. Scale bar: 20 μm.