Conclusion

A great deal of evidence supports an important role for the glutamatergic system in morphine withdrawal. The nonselective glutamate antagonist kynurenic acid can attenuate many symptoms of morphine withdrawal. Antagonists selective for NMDA and AMPA receptors can also attenuate many symptoms of morphine withdrawal. In addition, mGlu receptor group II receptor agonists, which can suppress the release of glutamate, can also attenuate many symptoms of opiate withdrawal. As NMDA antagonists may produce PCP-like side effects, AMPA receptor antagonists and mGlu group II receptor agonists may be novel pharmacotherapies in the treatment of opiate withdrawal in humans. There is also evidence for enhanced glutamate activity in select brain regions during morphine withdrawal. There is an increased release of glutamate in several brain regions during morphine withdrawal (e.g., LC, nucleus accumbens, spinal cord) and NMDA antagonists can block c-fos activation in several brain regions observed during morphine withdrawal (e.g., nucleus accumbens, amygdala). Activation of the LC during opiate withdrawal has been particularly well studied and is mediated primarily by increased release of glutamate acting at AMPA receptors. Taken together, these studies support the idea of morphine withdrawal as a state of glutamate hyperactivity in selected brain regions.

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