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Acute and subchronic administration of anandamide or oleamide increases REM sleep in rats.

机译:Anandamide或油酰胺的急性和亚慢性给药可增加大鼠的REM睡眠。

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摘要

Anandamide and oleamide, induce sleep when administered acutely, via the CB1 receptor. Their subchronic administration must be tested to demonstrate the absence of tolerance to this effect, and that the sudden withdrawal of these endocannabinoids (eCBs) does not affect sleep negatively. The sleep-waking cycle of rats was evaluated for 24h, under the effect of an acute or subchronic administration of eCBs, and during sudden eCBs withdrawal. AM251, a CB1 receptor antagonist (CB1Ra) was utilized to block eCBs effects. Our results indicated that both acute and subchronic administration of eCBs increase REMS. During eCBs withdrawal, rats lack the expression of an abstinence-like syndrome. AM251 was efficacious to prevent REMS increase caused by both acute and subchronic administration of these eCBs, suggesting that this effect is mediated by the CB1 receptor. Our data further support a role of the eCBs in REMS regulation.
机译:当通过CB1受体急性给药时,阿南酰胺和油酰胺会诱发睡眠。必须对其亚慢性给药进行测试,以证明对这种作用没有耐受性,并且突然停用这些内源性大麻素(eCBs)不会对睡眠产生负面影响。在急性或亚慢性给予eCB的影响下,以及在eCB突然戒断期间,评估了大鼠的觉醒周期24小时。利用CB1受体拮抗剂(CB1Ra)AM251来阻断eCB的作用。我们的结果表明,eCB的急性和亚慢性给药均可增加REMS。在eCB戒断期间,大鼠缺乏戒欲样综合征的表达。 AM251可以有效防止由这些eCB的急性和亚慢性给药引起的REMS升高,表明该作用是由CB1受体介导的。我们的数据进一步支持了eCB在REMS法规中的作用。

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