II) Electroconvulsive therapy.  Electroconvulsive therapy (ECT) is one of the most effective treatments for major depression, especially in subjects who do not respond to antidepressants, but its mechanisms of action remain largely unknown. Electroconvulsive seizure (ECS) differs from kindling and chemoconvulsant treatments in that it does not lead to an epileptiform state and does not cause cell death. ECS (one daily for 10 days) enhances (2 or 24 h after a BrdU pulse) cell proliferation in the DG, and the newly born cells survive for at least 3 mo, a time point when most of them express NeuN (75%) and few GFAP (13%) (331, 335). This proliferative effect is dose-dependent as a series of seizures further increases neurogenesis (331). The neurogenic efficacy of ECS has been investigated in conditions mimicking stress-induced depression, i.e., in animals with high corticosterone levels. The downregulation of neurogenesis (75%) in the GCL of rats chronically treated with corticosterone was eliminated by ECS performed at the end of the treatment (212). Because ECS upregulates several factors described as stimulating neurogenesis, such as bFGF, neuropeptide Y, VEGF, BDNF, and Cox-2 (404, 406), these factors are likely mediators of the proliferative effect of ECS. Among them, BDNF deserves special mention as ECS-induced MFS is diminished in BDNF knockout mice (549).