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在大鼠电刺激甩尾测痛模型上，应用鞘内注射（it）多巴胺（DA）受体选择性激动剂与拮抗剂，分析大鼠脊髓DA受体亚型D1和D2在痛及针刺镇痛（AA）中的作用。结果显示，在正常清醒大鼠，itD2受体选择性激动剂LY171555（LY）或D1／D2受体激动剂阿朴吗啡（APO）有镇痛作用（呈剂量依赖式增加），并加强AA，而itD1受体选择性激动剂SKF38393（SKF）对痛及AA均无影响；itD1受体选择性桔抗剂SCH23390（SCH）或D2受体选择性拮抗剂舒必利（Sul）均减弱AA的效应。结果提示，在脊髓水平，D2受体参与痛觉的调制，兴奋D2受体时有镇痛作用并增强AA；兴奋D1受体时显示不出参与作用，但阻断D1受体能抑制AA。
The rats were anesthetized with dopamine (DA) selective agonists and antagonists by applying an electric stimulation (tachycardia) dopamine (DA) receptor agonist and antagonist to rats. Analgesia (AA) in the role. The results showed that in normal awake rats, itD2 receptor selective agonist LY171555 (LY) or D1 / D2 receptor agonist apomorphine (APO) had analgesic effect (in a dose-dependent manner) and enhanced AA, However, itD1 receptor selective agonist SKF38393 (SKF) had no effect on pain and AA; itD1 receptor selective antagonist SCH23390 (SCH) or D2 receptor selective antagonist sulpiride attenuated the effect of AA. The results suggest that, at the spinal cord level, D2 receptors are involved in modulation of pain sensation, analgesic effect when excited by D2 receptors and potentiation of AA; excitability of D1 receptors is not involved, but blockade of D1 receptors inhibits AA.