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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Intrathecal N-methyl-D-aspartate (NMDA) induces paradoxical analgesia in the tail-flick test in rats.
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Intrathecal N-methyl-D-aspartate (NMDA) induces paradoxical analgesia in the tail-flick test in rats.

机译：鞘内注射N-甲基-D-天冬氨酸（NMDA）在大鼠的甩尾试验中引起矛盾的镇痛作用。

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The intrathecal (IT) administration of NMDA in rodents has usually been reported to produce hyperalgesic reactions, although some articles describe that spinal NMDA can lead to analgesia. We show here that the nociceptive behavior (biting, scratching, licking; BSL) observed after NMDA injection (1-8 microg/rat; IT) is followed by a long period of increased tail-flick latencies, not longer detected 24 h after NMDA administration. The NMDA-receptor antagonist CPP (10-100 ng/rat; IT) blocked the BSL behavior induced by NMDA. In the tail-flick test, this antagonist induced analgesia by itself, and was able, at 30 ng/rat, to prevent the NMDA-mediated analgesia. The implication of opiate mechanisms was discarded since naloxone (3 and 10 mg/kg; IP) did not antagonize NMDA-induced analgesia. Finally, the involvement of the intracellular calcium binding protein calmodulin was assessed. The calmodulin inhibitor, calmidazolium (30-300 microg/rat; IT) only blocked the excitatory effect (BSL) without modifying the tail-flick analgesia produced by NMDA (4 microg). These results show that a single intrathecal administration of NMDA sequentially induces both nociceptive and antinociceptive, nonopiate responses in rats.
机译：鞘内（IT）施用NMDA在啮齿动物中通常会产生痛觉过敏反应，尽管有些文章描述了脊柱NMDA可导致镇痛作用。我们在这里显示，NMDA注射后（1-8微克/大鼠; IT）观察到的伤害性行为（咬伤，抓挠，舔; BSL）后伴随着长时间的甩尾潜伏期，在NMDA后24小时不再检测到行政。 NMDA受体拮抗剂CPP（10-100 ng / rat; IT）阻断了NMDA诱导的BSL行为。在甩尾试验中，该拮抗剂本身可引起镇痛作用，并且以30 ng /大鼠的剂量能够预防NMDA介导的镇痛作用。由于纳洛酮（3和10 mg / kg; IP）不能拮抗NMDA诱导的镇痛作用，因此鸦片制剂的作用被放弃了。最后，评估了细胞内钙结合蛋白钙调蛋白的参与。钙调蛋白抑制剂，降钙净碱（30-300 microg / rat; IT）仅阻断了兴奋作用（BSL），而没有改变NMDA（4 microg）产生的甩尾镇痛作用。这些结果表明，鞘内单次施用NMDA可在大鼠中依次诱导伤害性和抗伤害性的非鸦片反应。

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