Foley Kelly A, Fudge Melissa A, Kavaliers Martin, Ossenkopp Klaus-Peter
Neuroscience Graduate Program, Psychology Department, Social Science Centre Room 7418, University of Western Ontario, London, Ont., Canada N6A 5C2.
Behav Brain Res. 2006 Feb 15;167(1):49-56. doi: 10.1016/j.bbr.2005.08.015. Epub 2005 Sep 27.
Sensitization of dopaminergic neural reward circuits has been hypothesized to be involved in the development of drug addiction. Highly palatable foods activate these same brain areas, specifically the nucleus accumbens. In this study, the effects of a highly palatable food (sucrose) on these circuits were investigated using the dopamine D(2)/D(3) receptor agonist quinpirole. Male Long-Evans rats received 30 min daily access to 0.3 M sucrose solution or water over nine consecutive days, followed by nine daily injections of quinpirole (0.5 mg/kg, s.c.) or saline. Locomotor activity was assessed using an automated open-field system. Locomotor sensitization developed, as quinpirole-treated rats traveled significantly more, and exhibited a greater number of movements than saline controls. A characteristic pattern of an initial suppression of locomotor activity, followed by excitation of activity was observed in quinpirole-treated rats. Pre-exposure to sucrose attenuated the initial suppression of activity, and facilitated excitation of activity. Rats that were pre-exposed to sucrose exhibited a reduced suppression of activity as compared to rats pre-exposed to water. Rats receiving sucrose and quinpirole also displayed a significantly greater enhancement of locomotor activity as compared to rats receiving water and quinpirole. These results support the hypothesis that highly palatable foods can alter the same neural reward circuits as drugs of abuse, and may facilitate sensitization-related addiction. This may aid in further understanding the neural basis of eating disorders.
多巴胺能神经奖赏回路的敏化被认为与药物成瘾的发展有关。高度可口的食物会激活这些相同的脑区,特别是伏隔核。在本研究中,使用多巴胺D(2)/D(3)受体激动剂喹吡罗研究了高度可口的食物(蔗糖)对这些回路的影响。雄性Long-Evans大鼠连续九天每天有30分钟接触0.3M蔗糖溶液或水的机会,随后九天每天注射喹吡罗(0.5mg/kg,皮下注射)或生理盐水。使用自动旷场系统评估运动活性。运动敏化出现了,因为接受喹吡罗治疗的大鼠比生理盐水对照组移动得明显更多,并且表现出更多的运动次数。在接受喹吡罗治疗的大鼠中观察到一种特征性模式,即最初运动活性受到抑制,随后活性被激发。预先接触蔗糖减弱了最初的活性抑制,并促进了活性激发。与预先接触水的大鼠相比,预先接触蔗糖的大鼠活性抑制有所降低。接受蔗糖和喹吡罗的大鼠与接受水和喹吡罗的大鼠相比,运动活性的增强也明显更大。这些结果支持了这样的假设,即高度可口的食物可以像滥用药物一样改变相同的神经奖赏回路,并可能促进与敏化相关的成瘾。这可能有助于进一步理解饮食失调的神经基础。