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CB1大麻素受体反向激动剂AM251对缺乏μ-阿片受体小鼠的食物摄入量和体重的影响。

Effects of the CB1 cannabinoid receptor inverse agonist AM251 on food intake and body weight in mice lacking mu-opioid receptors.

作者信息

Chen Richard Z, Frassetto Andrea, Fong Tung M

机构信息

Department of Metabolic Disorders, Merck Research Laboratories, P.O. Box 2000, RY80M-213, Rahway, NJ 07065, USA.

出版信息

Brain Res. 2006 Sep 7;1108(1):176-8. doi: 10.1016/j.brainres.2006.06.006. Epub 2006 Jul 7.

DOI:10.1016/j.brainres.2006.06.006
PMID:16828068
Abstract

We used mu-opioid receptor-deficient (MOR-/-) mice to determine the effects of the CB1 cannabinoid receptor inverse agonist AM251 on feeding in the absence of MOR signaling. A single dose of AM251 at 0.6, 2 or 6 mg/kg caused similar dose-dependent suppression of food intake in wild-type and MOR-/- mice. Administration of AM251 at 3 mg/kg/day for 9 consecutive days also led to a similar reduction ( approximately 8%) in body weight in wild-type and MOR-/- mice. Our results suggest that MOR signaling is not necessary for cannabinoid-mediated effects on feeding and that physiological antagonism of opioid receptor tone might be required for the observed synergistic effects of a CB1 inverse agonist and an opioid receptor antagonist on feeding.

摘要

我们使用μ-阿片受体缺陷（MOR-/-）小鼠来确定CB1大麻素受体反向激动剂AM251在缺乏MOR信号传导时对进食的影响。0.6、2或6mg/kg的单剂量AM251在野生型和MOR-/-小鼠中引起了相似的剂量依赖性食物摄入量抑制。连续9天每天给予3mg/kg的AM251也导致野生型和MOR-/-小鼠体重出现相似程度的下降（约8%）。我们的结果表明，MOR信号传导对于大麻素介导的进食影响并非必需，并且对于观察到的CB1反向激动剂和阿片受体拮抗剂对进食的协同作用而言，可能需要对阿片受体张力进行生理性拮抗。

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