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 XdUTP 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.
Keywords: Aging, experimental cerebral ischemia, caspase 3-TUNEL dual-labeling, neuroprotection, TUNEL
Current Neurovascular Research
Title: Aging is Neuroprotective During Global Ischemia but Leads to Increased Caspase-3 and Apoptotic Activity in Hippocampal Neurons
Volume: 3 Issue: 3
Author(s): Zhen He, James F. Meschia, Thomas G. Brott, Dennis W. Dickson and Michael Mckinney
Affiliation:
Keywords: Aging, experimental cerebral ischemia, caspase 3-TUNEL dual-labeling, neuroprotection, TUNEL
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 XdUTP 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.
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Cite this article as:
He Zhen, Meschia F. James, Brott G. Thomas, Dickson W. Dennis and Mckinney Michael, Aging is Neuroprotective During Global Ischemia but Leads to Increased Caspase-3 and Apoptotic Activity in Hippocampal Neurons, Current Neurovascular Research 2006; 3 (3) . https://dx.doi.org/10.2174/156720206778018802
DOI https://dx.doi.org/10.2174/156720206778018802 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
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