Figure 2
From: Sustained remission from depressive-like behavior depends on hippocampal neurogenesis
Neurogenesis arrest prevents long-term recovery from depression. (a) The relevance of neurogenesis for long-term recovery from depression was evaluated in animals exposed to an unpredictable chronic mild stress (uCMS) protocol 4 weeks before behavioral assessment. (b, c) Stress exposure triggers anhedonic behavior, that was reverted by fluoxetine and imipramine. Neurogenesis arrest with mehylazoxymethanol (MAM) in stressed animals precluded recovery from anhedonic signs in the sucrose consumption test (SCT). (d) Learned helplessness behavior, assessed in the forced swimming test (FST), was normalized after 4 weeks of spontaneous or antidepressant-induced recovery from stress. (e, f) The long-term recovery from anxiety-like behavior was prevented by neurogenesis arrest; fluoxetine anxiolytic effects were attenuated by MAM administration, while imipramine action remained unaffected. (g–j) Neurogenesis arrest prevented the recovery form cognitive deficits in (g) behavioral flexibility and in (h) working memory of animals exposed to uCMS; (i, j) the therapeutical action of fluoxetine on working memory was suppressed by MAM administration, while imipramine effect was maintained after neurogenesis arrest. Error bars denote s.e.m. *Denotes the effect of MAM; ⋄Denotes the effect of uCMS; #Denotes the antidepressants effect, by comparison of the antidepressants-treated animals with uCMS animals. *,⋄, #P<0.05, **,⋄⋄, ##P<0.01, ***,⋄⋄⋄, ###P<0.001; n=10–12 per group. EPM, elevated plus maze test; NSF, novelty-suppressed feeding test paradigm.
