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Modulation of ischemia-induced NMDAR1 activation by environmental enrichment decreases oxidative damage.

Abstract
In this study, we examined whether enriched environment (EE) housing has direct neuroprotective effects on oxidative damage following transient global cerebral ischemia. Fifty-two adult male Wistar rats were included in the study and received either ischemia or sham surgery. Once fully awake, rats in each group were randomly assigned to either: EE housing or socially paired housing (CON). Animals remained in their assigned environment for 7 days, and then were killed. Our data showed that glutamate receptor expression was significantly higher in the hippocampus of the ischemia CON group than in the ischemia EE group. Furthermore, the oxidative DNA damage, protein oxidation, and neurodegeneration in the hippocampus of the ischemia CON group were significantly increased compared to the ischemia EE group. These results suggest that EE housing possibly modulated the ischemia-induced glutamate excitotoxicity, which then attenuated the oxidative damage and neurodegeneration in the ischemia EE rats.
AuthorsTeresita L Briones, Magdalena Rogozinska, Julie Woods
JournalJournal of neurotrauma (J Neurotrauma) Vol. 28 Issue 12 Pg. 2485-92 (Dec 2011) ISSN: 1557-9042 [Electronic] United States
PMID21612313 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Retracted Publication)
Chemical References
  • NMDA receptor A1
  • Receptors, N-Methyl-D-Aspartate
Topics
  • Animals
  • Brain Ischemia (metabolism, prevention & control)
  • DNA Damage (physiology)
  • Environment
  • Hippocampus (metabolism)
  • Male
  • Oxidative Stress (physiology)
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate (metabolism)
  • Social Environment

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