Elsevier

Brain Research

Volume 553, Issue 2, 12 July 1991, Pages 327-330
Brain Research

MK-801 blocks the development of thermal hyperalgesia in a rat model of experimental painful neuropathy

https://doi.org/10.1016/0006-8993(91)90844-LGet rights and content

Abstract

Loose ligtiion of the sciatic nerve in the rat can produce behavioral signs of hyperalgesia in the hindpaw. This study examined the effect of an NMDA (N-methyl-d-aspartate) receptor antagonist (MK-801) on the development of hyperalgesia in this model. Rats received i.p. injections of saline of MK-801 (1.0 mg/kg) prior to and then for 7 days after a unilateral sciatic nerve ligation. Testing of each hindpaw for latency to withdrawal from astandardized thermal stimulus was performed prior to ligation and then at 10, 12, 17, 27, and 37 days postoperatively. Hyperalgesia of the operated hindpaw developed in saline-treated animals as measured by a decrease in withdrawal latency. Hyperalgesia did not develop in animals treated with MK-801. MK-801 may therefore prevent the development of hyperalgesia following experimental nerve injury, possibly through an NMDA receptor-mediated effect.

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    Citation Excerpt :

    In animal, NMDA receptor antagonists show controversial results. Neuropathic pain symptoms are decreased after treatment with MK801 (Davar et al., 1991; Mao et al., 1992, Smith et al., 1994), ketamine (Mao et al., 1993), dextromethorphan (Mao et al., 1993) or unchanged with MK801 (Wegert et al. 1997) and dextromethorphan (Tal and Bennett, 1994). These drugs may however have severe side-effects limiting their clinical use (Cvrcek, 2008).

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This work was supported by a National Research Service Award (NINDS Grant IF32NS085 34-02).

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The authors wish to acknowledge the support of Miriam Chernoff and Lee Baer of the Biostatistics Division at the Massachussetts General Hospital, and the support and encouragement of gary J. Bennett at the National Institutes of Dental Research, NIH.

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