Figure 1
From: Sustained remission from depressive-like behavior depends on hippocampal neurogenesis
Neurogenesis arrest induces long-term emotional and cognitive changes typical of depression. (a) Neurogenesis was arrested by methylazoxymethanol (MAM) administration and the effects on behavior were assessed after 4 weeks. MAM treatment decreased the number of BrdU-positive cells in the hippocampal dentate gyrus (b), that underwent neuronal (BrdU/NeuN) and astroglial (BrdU/GFAP) differentiation. (c) Deficits in proliferation were sustained 4 weeks after MAM treatment cessation. Behavioral phenotype was evaluated using a battery of tests to assess distinct behavioral domains affected in depression. (d, e) Long-term mood impairments were observed in the sucrose consumption test (SCT) (d), and in the forced swimming test (FST) (e) 4 weeks after MAM treatment. (f, g) Increased anxiety-like behavior was detected in the elevated plus maze test (EPM) (f) and in the novelty-suppressed feeding test paradigm (NSF) (g) in animals previously treated with MAM. (g, h) Cognitive performance was also affected 4 weeks after neurogenesis arrest, as both (h) working memory and (i) behavioral flexibility were impaired 4 weeks after MAM administration. MAM treatment did not affect the dendritic length of neither preexistent or newly born granule neurons (j), but there was a decrease in spine density in the dendrites of newly born neurons after MAM exposure. Error bars denote s.e.m. *P<0.05, **P<0.01, ***P<0.001; n=10–12 per group.
