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Delayed application of MK-801 attenuates development of morphine tolerance in rats

P Marek1, S Ben-Eliyahu, A L Vaccarino

  • 1Department of Psychology, University of California, Los Angeles 90024.

Brain Research
|August 30, 1991
PubMed

Insights

Blocking N-methyl-D-aspartic acid (NMDA) receptors with MK-801 significantly reduced morphine tolerance in rats. This suggests NMDA receptor changes are key to developing tolerance to morphine analgesia.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Pain Research

Background:

  • Morphine tolerance, a decreased response to the drug over time, is a significant clinical challenge.
  • The precise mechanisms underlying morphine tolerance are not fully understood.
  • N-methyl-D-aspartic acid (NMDA) receptors are implicated in various forms of neuronal plasticity and learning.

Purpose of the Study:

  • To investigate the role of NMDA receptor changes in the development of morphine tolerance.
  • To determine if antagonism of NMDA receptors can attenuate morphine tolerance.

Main Methods:

  • Rats received daily morphine injections for 4 days to induce tolerance.
  • The NMDA receptor antagonist MK-801 was administered 2 hours after morphine injections during the induction period.
  • Analgesia was assessed using the hot-plate test on the fifth day.

Main Results:

  • Administration of MK-801 significantly reduced the development of morphine tolerance.
  • The effect was observed even when MK-801 was given after morphine, ruling out state-dependent learning.

Conclusions:

  • Enduring or delayed changes at the NMDA receptor are likely involved in the mechanisms of morphine tolerance.
  • Targeting NMDA receptors may offer a therapeutic strategy to mitigate morphine tolerance.

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