Aging is neuroprotective during global ischemia but leads to increased caspase-3 and apoptotic activity in hippocampal neurons

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15 Scopus citations

Abstract

Previously, we found a significantly greater number of surviving CA1 neurons to global ischemia in the aged (24-month-old) F344 rats than in young (4-month-old) rats. The present study tests the hypothesis that aging retards neuronal death in the hippocampal CA1 region following cerebral ischemia. The CA1 "living cell ratio" was significantly greater in aged than in young rats at three days (62±8% vs. 30±8%) and at eight days (36±6% vs. 17±5%), but not at 14 days (15±12% vs. 18±12%) following ischemia. The number of the CA1 cells exhibiting co-localized TdT-mediated X-dUTP nick end labeling reaction and caspase-3 active peptide (C3AP) immunoreactivity was greater in aged than young animals at three and eight days following ischemia (36±8/mm vs. 3±1/mm and 36±14 vs. 0±0, p<0.05 respectively). Also, the total number of C3AP-positive cells in the CA1 region in the aged group was significantly greater than in the young group at three and eight days post-ischemia (p<0.05). Aging appears to delay caspase-3-dependent apoptotic cell death induced by global ischemia in the CA1 region of the hippocampus, consistent with an age-induced neuroprotective process.

Original languageEnglish (US)
Pages (from-to)181-186
Number of pages6
JournalCurrent Neurovascular Research
Volume3
Issue number3
DOIs
StatePublished - 2006

Keywords

  • Aging
  • Caspase 3-TUNEL dual-labeling
  • Experimental cerebral ischemia
  • Neuroprotection
  • TUNEL

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

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