Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Impairment of Synaptic Transmission by Transient Hypoxia in Hippocampal Slices: Improved Recovery in Glutathione Peroxidase Transgenic Mice

Denis Furling, Othman Ghribi, Ahmed Lahsaini, Marc-Edouard Mirault and Guy Massicotte
Proceedings of the National Academy of Sciences of the United States of America
Vol. 97, No. 8 (Apr. 11, 2000), pp. 4351-4356
Stable URL: http://www.jstor.org/stable/122158
Page Count: 6
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Impairment of Synaptic Transmission by Transient Hypoxia in Hippocampal Slices: Improved Recovery in Glutathione Peroxidase Transgenic Mice
Preview not available

Abstract

There is increasing evidence that oxygen free radicals contribute to ischemic brain injury. It is unclear, however, to what extent specific antioxidant enzymes can prevent or reverse the impairment of synaptic function caused by transient hypoxia. In this study, we investigated in transgenic (Tg) mice whether a moderate increase in glutathione peroxidase-1 (GPx1) may improve the capacity of CA1 pyramidal cells to recover synaptic transmission after a short period of hypoxia in vitro. In control hippocampal slices, transient hypoxia (7-9 min) produced irreversible loss of excitatory postsynaptic potentials. Complete recovery of synaptic transmission was observed with homozygous Tg-MT-GPx-6 mice after reoxygenation, and, after repeated episodes of hypoxia, synaptic transmission was still viable in most Tg slices, in contrast to non-Tg slices. Moreover, hypoxic episodes abolished the capacity of hippocampal slices to generate long-term potentiation in area CA1 of control mice, whereas a significant extent of long-term potentiation expression was still preserved in Tg tissues. We also demonstrated that susceptibility to N-methyl-D-aspartate-mediated oxidative injury was reduced in Tg hippocampal slices. In conclusion, our results suggest that a moderate GPx increase can be sufficient to prevent irreversible functional damage produced by transient hypoxia in the hippocampus and to help maintain basic electrophysiological mechanisms involved in memory formation.

Page Thumbnails

  • Thumbnail: Page 
4351
    4351
  • Thumbnail: Page 
4352
    4352
  • Thumbnail: Page 
4353
    4353
  • Thumbnail: Page 
4354
    4354
  • Thumbnail: Page 
4355
    4355
  • Thumbnail: Page 
4356
    4356