Figure 1.

Differential effects of mineralocorticoid receptor (MR)- and glucocorticoid receptor (GR)-activation on human hippocampal progenitor cell proliferation. 5′-bromodeoxyuridine (BrdU, 10 μℳ) incorporation and immunocytochemistry was used to assess proliferation of HPC03A/07 cells (a). Cortisol exerts bimodal, dose-dependent effects on proliferation (b). Spironolactone (1 μℳ) blocks the increase in cell proliferation upon treatment with low concentrations of cortisol (c). RU486 (50 nM) blocks the decrease in cell proliferation upon treatment with high concentrations of cortisol (100 μℳ) (d). The MR-agonist, aldosterone (1 nM–1 μℳ), increases cell proliferation (e), while the GR-agonist, dexamethasone (10 nℳ–5 μℳ), decreases cell proliferation (f). GR transactivation is dose-dependently increased by cortisol concentrations (10 μℳ–1 mℳ) (g). Three to four independent experiments were conducted on independent cultures (indicated as n). In proliferation experiments, 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; ***P<0.001 compared with the vehicle-treated control condition.