Human Adult Neurogenesis: Evidence and Remaining Questions

Renewed discussion about whether or not adult neurogenesis exists in the human hippocampus, and the nature and strength of the supporting evidence, has been reignited by two prominently published reports with opposite conclusions. Here, we summarize the state of the field and argue that there is currently no reason to abandon the idea that adult-generated neurons make important functional contributions to neural plasticity and cognition across the human lifespan

Stressing new neurons into depression?

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

Effect of aging on the basal expression of c-fos, c-jun, and egr-1 proteins in the hippocampus

International audienceIn the present study the effect of aging on the basal expression of three different immediate early genes (IEGs) was investigated. The protein products of c-fos, c-jun, and egr-1 genes were visualized immunohistochemically in the rat hippocampus of young adult (4-month-old) and old rats (20-month-old). Astrocytes were quantified by GFAp immunostaining to determine whether changes in the expression of IEGs were correlated with modifications in this marker of degenerative changes. In the young adult rat brain, basal levels of c-Jun and Egr-1 but not c-Fos were detected within the hippocampal formation. Whereas very high basal levels of c-Jun were found in the dentate granule cells and in the pyramidal cells of the ventral hippocampus, Egr-1 was highly expressed in the CA1 pyramidal cells of the dorsal hippocampus. Aging was accompanied by a decrease in Egr-1 expression, by a decrease in total cell density, as well as by a loss of astrocytes in CA1 subfields. In contrast, basal expression of c-Fos and c-Jun as well as astrocyte density within the dentate gyrus were not affected by aging. No difference in these markers was observed in aged rats with or without impairment in spatial learning in a water maze. It was concluded that although these changes may reflect senescence-induced decline of brain function, they do not constitute the defect underlying the age-associated reduction in mnesic capability