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. 2018 Jan 29;8:1829. doi: 10.1038/s41598-018-20271-x

Figure 4.

Figure 4

Activation of α7-nAChR in gp120-tgm striatal neurons leads to apoptosis. Striatal neurons from WT, and gp120-tgm mice were incubated with ACh (1 hr) to activate α7-nAChR or with a pretreatment of Bgtx (30 min) and then ACh (1 hr) to block α7-nAChR function. Cells were labeled with Annexin-V and Propidium Iodide (PI) to measure those undergoing apoptosis processes. (A) The percentage of striatal neurons labeled with Annexin-V and PI was quantified. White bars represent results for WT striatal neurons, red for gp120-tgm. Activation of α7-nAChR with ACh exacerbated the condition on gp120-tgm striatal neurons where the percentage of apoptotic cells doubles, an effect attenuated by Bgtx preincubation. (B) In a separate experiment, WT and gp120-tgm were trained to perform a delayed non-matching (DNM) paradigm, to assess striatum-dependent behavioral differences. The experimental phase lasted for 5 days. Since day one, except for day two, gp120-tgm consistently performed poorer than WT mice, suggesting striatal-dependent cognitive impairment as early as 4-months of age. Results are shown as mean ± SEM values. Two-Way ANOVA for apoptosis assays, n = 5 mice/strain, *P ≤ 0.05, scale bar = 20 μm. Two-Way ANOVA for behavioral test, n = 6 for WT and n = 5 for gp120-tgm, **P ≤ 0.001, ***P ≤ 0.0001.