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. 2021 Dec 15;41(50):10365–10381. doi: 10.1523/JNEUROSCI.1475-21.2021

Figure 2.

Figure 2.

17αE2 protects against HIV-1 gp120-induced dendritic damage. A, B, MAP2 staining (top; scale bar, 20 µm) and GFP expression (bottom; scale bar, 10 µm) in primary hippocampal neurons (DIV 15) after treatment with HIV-1 gp120 (0.2–1 nm for 48 h). HIV-1 gp120, in a concentration-dependent manner, decreased dendritic length and dendritic spine density. C, D, Time-lapse confocal images show the rapid changes in spine structure of the same dendrite at 0 and 10 min following HIV-1 gp120 treatment (0.5 nm) in the absence and presence of 17αE2 (10 nm, 10 min pretreatment) in mouse hippocampal neurons (DIV 12–14) transduced with GFP. Filled arrowheads indicate spine growth and formation, while open arrowheads indicate spine elimination and/or reduction between the two time points. Scale bar, 10 µm. Percentage changes in dendritic spine turnover and spine volume over 10 min with different treatments are shown in D. Positive values indicate spine formation, while negative values indicate spine elimination between 0 and 10 min. E, Quantification of dendritic spine morphology in fixed neurons following HIV-1 gp120 treatment (0.5 nm for 30 min) in the absence and presence of 17αE2 (10 nm, 10 min pretreatment). F, Confocal images show changes in the distribution of ERα-GFP in response to 17αE2 (10 nm for 30 min) in CLU199 cells costained with DAPI for nucleus. G, Quantitative change of nuclear ER activation in response of HIV-1 gp120 (0.5 nm for 30 min) or 17αE2 (10 nm for 30 min) using estrogen receptor transcription factor ELISA (TransAM-ER).