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Four weeks after a priming stressful event, serum corticosterone concentration returned to control values in all animals, whereas the other biological parameters returned to basal level in only 58% of animals (called nonvulnerable). In contrast, 42% of animals displayed persistent decreased serum and hippocampus BDNF concentrations, reduced hippocampal volume and neurogenesis, CA3 dendritic retraction and decrease in spine density, as well as amygdala neuron hypertrophy, constituting latent vulnerability traits to depression. In this group, called vulnerable, a subsequent mild stress evoked a rise of serum corticosterone levels and a \u201cdepressive\u201d phenotype, in contrast to nonvulnerable animals. Intracerebroventricular administration of 7,8-dihydroxyflavone, a selective TrkB receptor agonist, dampened the development of the \u201cdepressive\u201d phenotype. Our results thus characterize the presence of latent vulnerability traits that underlie the emergence of depression and identify the association of low BDNF with normal corticosterone serum concentrations as a predictive biomarker of vulnerability to depression.<\/jats:p>","DOI":"10.1523\/jneurosci.1309-11.2011","type":"journal-article","created":{"date-parts":[[2011,9,7]],"date-time":"2011-09-07T14:54:38Z","timestamp":1315407278000},"page":"12889-12899","source":"Crossref","is-referenced-by-count":163,"title":["Vulnerability to Depression: From Brain Neuroplasticity to Identification of 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