Abstract
A key question in the field of neurogenesis, stress and depression has been whether a reduction in neurogenesis per se can produce a ‘depressed’ animal. Recently, Snyder et al. convincingly demonstrated that new hippocampal neurons are necessary for an efficient recovery of hypothalamic-pituitary-adrenal (HPA) axis activity after stress. They next proposed a feed-forward loop by which stress, via inhibition of neurogenesis, could over time, lead to hypercortisolemia and eventually depressive behavior. Although we applaud their results, we consider it too early to conclude that neurogenesis controls the stress response; nor do they, in our view, support a causal role for neurogenesis in depression.
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