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The Journal of Neuroscience, January 1, 2003, 23(1):269-276

Hydrogen Peroxide Modulation of Synaptic Plasticity

Ariel Kamsler and Menahem Segal

Department of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel

Unlike the proposed role of reactive oxygen species in neurodegeneration, acute effects of reactive oxygen on synaptic plasticity are poorly understood. Using rat hippocampal slices, we found that exposure to a high concentration (0.5-5 mM) of H₂O₂ reduces EPSPs in both potentiated and nonpotentiated synapses. Exposure of the slices to 20 µM H₂O₂ did not affect expression of preestablished long-term potentiation (LTP) but prevented induction of new LTP and enhanced long-term depression (LTD). Surprisingly, 1 µM H₂O₂ caused a twofold increase in LTP compared with controls, and it further enhanced NMDA-independent LTP. A low concentration of H₂O₂ also suppressed LTD. Nifedipine, an L-type calcium channel blocker, did not affect control LTP but blocked effects of both 1 and 20 µM H₂O₂. Calcineurin inhibitors [FK506 (FR900506) and cyclosporin A but not rapamycin] acted similarly and also restored LTP in the presence of 20 µM H₂O₂. These results suggest that H₂O₂ alters NMDA-independent, voltage-gated calcium channel-mediated LTP by activating calcineurin.

Key words: calcineurin; hippocampus; LTP; LTD; calcium; hydrogen peroxide

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Copyright © 2003 Society for Neuroscience  0270-6474/03/231269-08$05.00/0

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