Dysregulation of brain reward systems in eating disorders: neurochemical information from animal models of binge eating, bulimia nervosa, and anorexia nervosa.
Dysregulation of brain reward systems in eating disorders: neurochemical information from animal models of binge eating, bulimia nervosa, and anorexia nervosa.
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DOI：
10.1016/j.neuropharm.2011.11.010
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发表时间：
2012-07
影响因子：
4.7
通讯作者：
Bocarsly ME
中科院分区：
文献类型：
--
作者：
Avena NM;Bocarsly ME
食物的摄入在一定程度上是通过大脑的激励和强化途径来调节的。这些通路的失调可能是饮食失调患者表现出的一些行为的基础。利用进食障碍的动物模型进行的研究极大地促进了对潜在大脑机制的详细研究，其中许多机制是异常进食行为的原因或后果的基础。这篇综述集中在通过暴食、神经性暴食症或神经性厌食症的动物模型获得的奖赏相关脑功能障碍的神经化学证据。这一发现表明，与奖励相关的大脑区域的多巴胺(DA)、乙酰胆碱(ACh)和阿片系统的变化是对暴饮暴食的反应。此外，神经性暴食症的动物模型表明，虽然暴饮暴食会释放DA，但通便会减弱ACh的释放，否则ACh可能会发出饱腹感的信号。神经性厌食症的动物模型表明，当动物进食时，限制获取食物的途径会增强DA的强化作用。基于活动的厌食症模型表明，中脑边缘多巴胺和5-羟色胺的变化是由于饥饿和过度的车轮跑步造成的。这些发现与动物模型补充了通过临床人群的神经成像和药物治疗研究获得的数据。最后，关于与这些进食障碍相关的行为的神经化学后果的信息将有助于理解这些复杂的障碍，并可能为未来的治疗方法提供信息，如本文所讨论的。
Food intake is mediated, in part, through brain pathways for motivation and reinforcement. Dysregulation of these pathways may underlay some of the behaviors exhibited by patients with eating disorders. Research using animal models of eating disorders has greatly contributed to the detailed study of potential brain mechanisms that many underlie the causes or consequences of aberrant eating behaviors. This review focuses on neurochemical evidence of reward-related brain dysfunctions obtained through animal models of binge eating, bulimia nervosa, or anorexia nervosa. The findings suggest that alterations in dopamine (DA), acetylcholine (ACh) and opioid systems in reward-related brain areas occur in response to binge eating of palatable foods. Moreover, animal models of bulimia nervosa suggest that while bingeing on palatable food releases DA, purging attenuates the release of ACh that might otherwise signal satiety. Animal models of anorexia nervosa suggest that restricted access to food enhances the reinforcing effects of DA when the animal does eat. The activity-based anorexia model suggests alterations in mesolimbic DA and serotonin occur as a result of starvation coupled with excessive wheel running. These findings with animal models complement data obtained through neuroimaging and pharmacotherapy studies of clinical populations. Finally, information on the neurochemical consequences of the behaviors associated with these eating disorders will be useful in understanding these complex disorders and may inform future therapeutic approaches, as discussed here.