Figure 1
From: Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor
Antidepressants induce differentiation and neuronal maturation of HPC03A/07 human hippocampal progenitor cells. Immunocytochemistry (ICC) for doublecortin (Dcx) and microtubulin-associated protein-2 (MAP2) was used to assess neuronal differentiation and maturation, respectively. 5′-bromodeoxyuridine (BrdU) incorporation and immunocytochemistry were used to assess progenitor cell proliferation (a). When HPC03A/07 cells were treated during the proliferation phase (72 h) and the subsequent differentiation phase (7 days), drug treatment had a significant effect on MAP2-positive neurons (one-way analysis of variance, P<0.0001, F1,4=62.22, R2=0.9120, n=5) and on Dcx-positive neuroblasts (one-way analysis of variance, P=0.0007, F1,4=13.28, R2=0.6713, n=5). Sertraline (SERT, 1 μM) increased the number of MAP2-positive neurons but did not alter the number of Dcx-positive neuroblasts, whereas dexamethasone (DEX, 1 μM) decreased both. No effect was observed upon co-treatment with SERT and DEX (b). When HPC03A/07 cells were treated only during the proliferation phase, drug treatment had a significant effect on MAP2-positive neurons (one-way analysis of variance, P=0.0022, F1,4=9.764, R2=0.5824, n=5) and on Dcx-positive neuroblasts (one-way analysis of variance, P<0.0001, F1,4=44.44, R2=0.8724, n=5). SERT increased the number of Dcx-positive neuroblasts, without an effect on MAP2-positive neurons (c). Treatment only during the differentiation phase did not have an effect on MAP2-positive neurons (one-way analysis of variance, P=0.5699, F1,4=0.6184, R2=0.1709, n=5) or on Dcx-positive neuroblasts (one-way analysis of variance, P=0.2146, F1,4=2.127, R2=0.4596, n=5) (d). Five independent experiments were conducted on five independent cultures (n=5), four wells were analyzed per treatment condition in each experiment and three random, non-overlapping pictures were analyzed for each well. All data are mean±s.e.m. *P<0.05, **P<0.01 and ***P<0.001 compared with the corresponding vehicle-treated control.
