Present address: Synaptic plasticity laboratory, Queensland Brain Institute, Saint Lucia, Australia
Reversal of age-related oxidative stress prevents hippocampal synaptic plasticity deficits by protecting d-serine-dependent NMDA receptor activation
Article first published online: 1 FEB 2012
© 2012 The Authors. Aging Cell © 2012 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland
Volume 11, Issue 2, pages 336–344, April 2012
How to Cite
Haxaire, C., Turpin, F. R., Potier, B., Kervern, M., Sinet, P.-M., Barbanel, G., Mothet, J.-P., Dutar, P. and Billard, J.-M. (2012), Reversal of age-related oxidative stress prevents hippocampal synaptic plasticity deficits by protecting d-serine-dependent NMDA receptor activation. Aging Cell, 11: 336–344. doi: 10.1111/j.1474-9726.2012.00792.x
- Issue published online: 15 MAR 2012
- Article first published online: 1 FEB 2012
- Accepted manuscript online: 9 JAN 2012 04:10PM EST
- Accepted for publication 1 January 2012
Fig. S1 Long-term dietary treatment with L-NAC prevents the age-dependent increase in carbonylated proteins.
Fig. S2 Acute L-NAC does not affect isolated NMDA-R-mediated synaptic potentials in young animals.
Fig. S3 Age-related astrogliosis persists in the hippocampus of aged rats after long-term dietary treatment with L-NAC.
Fig. S4 Long-term dietary treatment with L-NAC prevents age-related decrease in d-serine levels.
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