Fig. 2: Acute 17β-estradiol (E2) treatment restores dendritic spine density following long term DISC1 knockdown.
From: Estradiol reverses excitatory synapse loss in a cellular model of neuropsychiatric disorders
a, b Western blot of hEK293 cells expressing HA-DISC1 in presence of control shRNA vector (pGSuper) or DISC1-shRNA (a). Quantification of HA-DISC1 expression (b), normalized to β-actin demonstrates that DISC1_shRNA effectivity knockdown exogenous DISC1 as previously reported. c Representative images of cortical neurons expressing control shRNA vector (pGSuper) or shRNA against DISC1 (DISC1_shRNA) for 7 days; neurons were treated with vehicle (Veh) or E2 (10 nM) for 30 min. d Quantification of dendritic spine linear density (per 10 µm). As recently reported, expression of DISC1_shRNA for 7 days resulted in a reduction in spine linear density; as expected 30 min E2 increases spine density in control neurons. Intriguingly, E2 treatment for 30 min increased spine density in DISC1_shRNA expressing cells to control neuron levels (dendritic spine linear density (per 10 µm): control, 5.1 ± 0.3; control + 17β-estradiol, 7.25 ± 0.49; DISC1_shRNA, 3.4 ± 0.35; DISC1_shRNA + 17β-estradiol, 4.95 ± 0.27). Scale bar = 5 µm.
