Lifelong corticosterone level determines age-related decline in neurogenesis and memory

M. F. Montaron, E. Drapeau, D. Dupret, P. Kitchener, C. Aurousseau, M. Le Moal, P. V. Piazza, D. N. Abrous

Research output: Contribution to journalArticlepeer-review

166 Scopus citations

Abstract

Ageing is accompanied by an alteration of spatial memory, a decline in hippocampal neurogenesis and a dysregulation of the hypothalamic-pituitary axis (HPA) leading to elevated levels of circulating corticosterone. However, the role of the HPA axis in age-related decline in cognitive functions and in neurogenesis decline remains unclear. We found that suppression of glucocorticoids secretion from midlife to the rest of the animals' life increases neurogenesis in old animals and prevents the emergence of age-related memory disorders. Reciprocally, aged rats with a chronic upregulation of the HPA axis exhibit not only spatial memory impairments but also very low levels of hippocampal cell proliferation and survival. Altogether, these results indicate that the extent of lifetime exposure to glucocorticoids determines the extent of age-related decline in hippocampal neurogenesis and consequently age-related cognitive dysfunctions.

Original languageEnglish
Pages (from-to)645-654
Number of pages10
JournalNeurobiology of Aging
Volume27
Issue number4
DOIs
StatePublished - Apr 2006
Externally publishedYes

Keywords

  • Ageing
  • Corticosterone
  • Hippocampus
  • Neurogenesis
  • Spatial learning

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