Cannabinoid agonists and antagonists modulate lithium-induced conditioned gaping in rats.

Linda A Parker, Raphael Mechoulam
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引用次数: 51

Abstract

Considerable evidence indicates that conditioned gaping in rats reflects nausea in this species that does not vomit. A series of experiments evaluated the potential of psychoactive cannabinoid agonists, delta-9-THC and HU-210, and non-psychoactive cannabinoids, Cannabidiol (CBD) and its dimethylheptyl homolog (CBD-dmh), to interfere with the establishment and the expression of conditioned gaping in rats. All agents attenuated both the establishment and the expression of conditioned gaping. Furthermore, the CB1 antagonist, SR-141716, reversed the suppressive effect of HU-210 on conditioned gaping. Finally, SR-141716 potentiated lithium-induced conditioned gaping, suggesting that the endogenous cannabinoid system plays a role in the control of nausea.

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大麻素激动剂和拮抗剂调节大鼠锂诱导的条件性间隙。
相当多的证据表明,大鼠的条件性张开反应了这种不呕吐的物种的恶心。一系列实验评估了精神活性大麻素激动剂δ -9- thc和HU-210以及非精神活性大麻素大麻二酚(CBD)及其二甲基庚基同源物(CBD-dmh)对大鼠条件开口的建立和表达的影响。所有药剂均能减弱条件性裂口的形成和表达。此外,CB1拮抗剂SR-141716逆转了HU-210对条件开口的抑制作用。最后,SR-141716增强了锂诱导的条件张口,表明内源性大麻素系统在恶心的控制中起作用。
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