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THERE is previous evidence suggesting that nerve injury-induced activation of N-methyhaspartate (NMDA) receptors might cause intracellular changes, providing a mechanism for chronic pain.' To test this hypothesis, we used an experimental model of neuropathy induced by spinal nerve ligation to investigate the preemptive effect of a noncompetitive NMDA receptor antagonist, MK-801, on tactile allodynia and mechanical hyperalgesia.
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Wei et al. (1999) studied this question.
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