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首页> 外文期刊>Life sciences >Endogenous cannabinoid receptor agonist anandamide induces peripheral antinociception by activation of ATP-sensitive K+ channels.
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Endogenous cannabinoid receptor agonist anandamide induces peripheral antinociception by activation of ATP-sensitive K+ channels.

机译：内源性大麻素受体激动剂anandamide通过激活ATP敏感的K +通道诱导外周镇痛作用。

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AIMS: The effects of several potassium (K(+)) channel blockers were studied to determine which K(+) channels are involved in peripheral antinociception induced by the cannabinoid receptor agonist, anandamide. MAIN METHODS: Hyperalgesia was induced by subcutaneous injection of 250 mug carrageenan into the plantar surface of the hind paw of rats. The extent of hyperalgesia was measured using a paw pressure test 3 h following carrageenan injection. The weight in grams (g) that elicited a nociceptive response, paw flexion, during the paw pressure test was used as the nociceptive response threshold. KEY FINDINGS: Doses of 50, 75, and 100 ng of anandamide elicited a dose-dependent antinociceptive effect. Following a 100 ng dose of anandamide no antinociception was observed in the paw that was contralateral to the anandamide injection site, which shows that anandamide has a peripheral site of action. Pretreatment with 20, 40 and 80 mug AM251, a CB(1) receptor antagonist, caused a dose-dependent decrease in anandamide-induced antinociception, suggesting that the CB(1) receptor is directly involved in anandamide effect. Treatment with 40, 80 and 160 mug glibenclamide, an ATP-sensitive K(+) channel blocker, caused a dose-dependent reversal of anandamide-induced peripheral antinociception. Treatment with other K(+) channel antagonists, tetraethylammonium (30 mug), paxilline (10 mug) and dequalinium (50 mug), had no effect on the induction of peripheral antinociception by anandamide. SIGNIFICANCE: This study provides evidence that the peripheral antinociceptive effect of the cannabinoid receptor agonist, anandamide, is primarily caused by activation of ATP-sensitive K(+) channels and does not involve other potassium channels.
机译：目的：研究了几种钾（K（+））通道阻滞剂的作用，以确定哪些K（+）通道参与了由大麻素受体激动剂anandamide诱导的外周镇痛作用。主要方法：通过向大鼠后爪的足底表面皮下注射250杯角叉菜胶来诱导痛觉过敏。在注射角叉菜胶后3小时，用爪压力试验测量痛觉过敏的程度。在脚掌压力测试过程中引起伤害性反应（爪弯曲）的重量（克）（g）用作伤害性反应阈值。主要发现：剂量分别为50、75和100 ng的anandamide引起剂量依赖性抗伤害感受作用。服用100 ng剂量的anandamide后，在与anandamide注射部位对侧的脚掌中未观察到抗伤害感受，这表明anandamide具有外围作用部位。用20、40和80马克杯AM251（一种CB（1）受体拮抗剂）进行预处理会导致剂量依赖性地减少anandamide诱导的抗伤害感受，这表明CB（1）受体直接参与anandamide的作用。用40、80和160马克杯的格列本脲（一种ATP敏感的K（+）通道阻滞剂）治疗，引起剂量依赖性的anandamide诱导的外周镇痛作用的逆转。用其他K（+）通道拮抗剂，四乙铵（30马克杯），paxilline（10马克杯）和去甲乙铵（50马克杯）治疗对anandamide诱导的外周抗伤害感受没有作用。意义：这项研究提供了证据表明大麻素受体激动剂anandamide的外周镇痛作用主要是由ATP敏感性K（+）通道的激活引起的，并且不涉及其他钾通道。

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