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An analgesia circuit activated by cannabinoids.

机译：由大麻素激活的镇痛回路。

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Although many anecdotal reports indicate that marijuana and its active constituent, delta-9-tetrahydrocannabinol (delta-9-THC), may reduce pain sensation, studies of humans have produced inconsistent results. In animal studies, the apparent pain-suppressing effects of delta-9-THC and other cannabinoid drugs are confounded by motor deficits. Here we show that a brainstem circuit that contributes to the pain-suppressing effects of morphine is also required for the analgesic effects of cannabinoids. Inactivation of the rostral ventromedial medulla (RVM) prevents the analgesia but not the motor deficits produced by systemically administered cannabinoids. Furthermore, cannabinoids produce analgesia by modulating RVM neuronal activity in a manner similar to, but pharmacologically dissociable from, that of morphine. We also show that endogenous cannabinoids tonically regulate pain thresholds in part through the modulation of RVM neuronal activity. These results show that analgesia produced by cannabinoids and opioids involves similar brainstem circuitry and that cannabinoids are indeed centrally acting analgesics with a new mechanism of action.
机译：尽管许多传闻表明大麻及其活性成分delta-9-tetrahydrocannabinol（delta-9-THC）可能会减轻疼痛感，但对人体的研究却产生了不一致的结果。在动物研究中，delta-9-THC和其他大麻素药物的明显镇痛作用与运动功能障碍混淆。在这里，我们显示大麻素的镇痛作用也需要有助于吗啡止痛作用的脑干回路。延髓延髓腹腔（RVM）的失活可防止止痛，但不能全身给药大麻素而产生运动功能障碍。此外，大麻素以类似于吗啡的药理学上可分离的方式通过调节RVM神经元活性来产生镇痛作用。我们还显示，内源性大麻素部分通过RVM神经元活性的调节来调节疼痛阈值。这些结果表明，由大麻素和阿片类药物产生的镇痛作用涉及相似的脑干回路，并且大麻素确实是具有新作用机制的中枢镇痛药。

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