在CB1受体缺失的小鼠中，暴饮暴食、酒精和蔗糖的摄入量减少。
Overeating, alcohol and sucrose consumption decrease in CB1 receptor deleted mice.
作者信息
Poncelet Martine, Maruani Jeanne, Calassi Roselyne, Soubrié Philippe
机构信息
Central Nervous System Department, Sanofi-Synthélabo Recherche, 371 rue du Professeur Joseph Blayac, 34184 Montpellier Cedex 04, France.
出版信息
Neurosci Lett. 2003 Jun 12;343(3):216-8. doi: 10.1016/s0304-3940(03)00397-5.
Administration of the cannabinoid CB1 receptor antagonist SR141716 (3-10 mg/kg i.p.) abolished neuropeptide Y-induced overeating and significantly reduced ethanol and sucrose intake in CB1 wild-type (+/+) mice. In CB1 receptor knockout (-/-) mice, neuropeptide Y totally lost its capacity to increase food consumption. Similarly, sucrose and ethanol intakes were significantly lower in CB1-/- vs. CB1+/+ mice. In CB1 deficient mice, SR141716 had no effect in these models.
给予大麻素CB1受体拮抗剂SR141716（腹腔注射3 - 10毫克/千克）可消除神经肽Y诱导的暴饮暴食，并显著降低CB1野生型（+/+）小鼠的乙醇和蔗糖摄入量。在CB1受体基因敲除（-/-）小鼠中，神经肽Y完全丧失了增加食物摄入量的能力。同样，CB1 - / - 小鼠的蔗糖和乙醇摄入量明显低于CB1 + / + 小鼠。在CB1缺乏的小鼠中，SR141716在这些模型中没有效果。
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