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Abstract
There is a growing body of evidence demonstrating that stress decreases the expression
of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood
and that antidepressant treatment reverses or blocks the effects of stress. Decreased
levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy
of certain limbic structures, including the hippocampus and prefrontal cortex that
has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants
could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic
actions of these treatments. This review provides a critical examination of the neurotrophic
hypothesis of depression that has evolved from this work, including analysis of preclinical
cellular (adult neurogenesis) and behavioral models of depression and antidepressant
actions, as well as clinical neuroimaging and postmortem studies. Although there are
some limitations, the results of these studies are consistent with the hypothesis
that decreased expression of BDNF and possibly other growth factors contributes to
depression and that upregulation of BDNF plays a role in the actions of antidepressant
treatment.