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[NMDA receptor and long-term potentiation]

H Gozlan1, D Diabira, P Chinestra

  • 1INSERM U. 29, Hôpital de Port-Royal, Paris, France.

Comptes Rendus De L'Academie Des Sciences. Serie III, Sciences De La Vie
|October 1, 1994
PubMed
Summary

The NMDA receptor redox site is crucial for long-term potentiation (LTP). Redox agents like DTNB and TCEP modulate LTP, suggesting potential therapeutic applications for conditions like cerebral ischemia.

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Area of Science:

  • Neuroscience
  • Neurochemistry

Background:

  • The N-methyl-D-aspartate (NMDA) receptor plays a key role in synaptic plasticity, including long-term potentiation (LTP).
  • The redox site on the NMDA receptor is implicated in modulating its function.

Purpose of the Study:

  • To investigate the role of the NMDA receptor redox site in the induction and expression of LTP.
  • To examine the effects of thiol-oxidizing (DTNB) and disulfide-reducing (TCEP) agents on NMDA receptor-dependent LTP.

Main Methods:

  • Utilized electrophysiological recordings to assess LTP in the presence of DTNB and TCEP.
  • Investigated the impact of these redox agents on both the induction and expression phases of LTP.
  • Examined effects on AMPA receptor-mediated synaptic transmission.

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Main Results:

  • DTNB, a thiol-oxidizing agent, irreversibly reduced NMDA receptor EPSP by 50% and prevented the induction of tetanic and anoxic LTP.
  • DTNB reversed established tetanic and anoxic LTP, while TCEP restored it.
  • These redox agents did not affect AMPA synaptic transmission or AMPA-LTP.

Conclusions:

  • The NMDA receptor redox site is critical for LTP induction and expression.
  • Modulation of this redox site offers a potential therapeutic strategy for cerebral ischemia.
  • Thiol-oxidizing compounds may hold promise for treating conditions involving excitotoxicity.