Adan R A H, Hillebrand J J G, Danner U N, Cardona Cano S, Kas M J H, Verhagen L A W
Department of Neuroscience and Pharmacology, Rudolf Magnus Institute of Neuroscience, University Medical Centre, Utrecht, The Netherlands.
Curr Top Behav Neurosci. 2011;6:229-50. doi: 10.1007/7854_2010_77.
Hyperactivity in anorexia nervosa is difficult to control and negatively impacts outcome. Hyperactivity is a key driving force to starvation in an animal model named activity-based anorexia (ABA). Recent research has started unraveling what mechanisms underlie this hyperactivity. Besides a general increase in locomotor activity that may be an expression of foraging behavior and involves frontal brain regions, the increased locomotor activity expressed before food is presented (food anticipatory behavior or FAA) involves hypothalamic neural circuits. Ghrelin plays a role in FAA, whereas decreased leptin signaling is involved in both aspects of increased locomotor activity. We hypothesize that increased ghrelin and decreased leptin signaling drive the activity of dopamine neurons in the ventral tegmental area. In anorexia nervosa patients, this altered activity of the dopamine system may be involved not only in hyperactivity but also in aberrant cognitive processing related to food.
神经性厌食症中的多动难以控制，且会对治疗结果产生负面影响。在一种名为基于活动的厌食症（ABA）的动物模型中，多动是导致饥饿的关键驱动力。最近的研究已开始揭示这种多动背后的机制。除了可能作为觅食行为表现且涉及额叶脑区的运动活动普遍增加外，在呈现食物之前表现出的运动活动增加（食物预期行为或FAA）涉及下丘脑神经回路。胃饥饿素在FAA中起作用，而瘦素信号减少则与运动活动增加的两个方面都有关。我们假设，胃饥饿素增加和瘦素信号减少会驱动腹侧被盖区多巴胺神经元的活动。在神经性厌食症患者中，多巴胺系统这种改变的活动可能不仅与多动有关，还与食物相关的异常认知加工有关。
