Robinson Mike J F, Burghardt Paul R, Patterson Christa M, Nobile Cameron W, Akil Huda, Watson Stanley J, Berridge Kent C, Ferrario Carrie R
1] Department of Psychology, University of Michigan, Ann Arbor, MI, USA [2] Department of Psychology, Wesleyan University, Middletown, CT, USA.
1] Molecular and Behavioral Neuroscience Institute, The University of Michigan School of Medicine, Ann Arbor, MI, USA [2] Department of Psychiatry, University of Michigan School of Medicine, Ann Arbor, MI, USA.
Neuropsychopharmacology. 2015 Aug;40(9):2113-23. doi: 10.1038/npp.2015.71. Epub 2015 Mar 12.
Pavlovian cues associated with junk-foods (caloric, highly sweet, and/or fatty foods), like the smell of brownies, can elicit craving to eat and increase the amount of food consumed. People who are more susceptible to these motivational effects of food cues may have a higher risk for becoming obese. Further, overconsumption of junk-foods leading to the development of obesity may itself heighten attraction to food cues. Here, we used a model of individual susceptibility to junk-foods diet-induced obesity to determine whether there are pre-existing and/or diet-induced increases in attraction to and motivation for sucrose-paired cues (ie, incentive salience or 'wanting'). We also assessed diet- vs obesity-associated alterations in mesolimbic function and receptor expression. We found that rats susceptible to diet-induced obesity displayed heightened conditioned approach prior to the development of obesity. In addition, after junk-food diet exposure, those rats that developed obesity also showed increased willingness to gain access to a sucrose cue. Heightened 'wanting' was not due to individual differences in the hedonic impact ('liking') of sucrose. Neurobiologically, Mu opioid receptor mRNA expression was lower in striatal 'hot-spots' that generate eating or hedonic impact only in those rats that became obese. In contrast, prolonged exposure to junk-food resulted in cross-sensitization to amphetamine-induced locomotion and downregulation of striatal D2R mRNA regardless of the development of obesity. Together these data shed light on individual differences in behavioral and neurobiological consequences of exposure to junk-food diets and the potential contribution of incentive sensitization in susceptible individuals to greater food cue-triggered motivation.
与垃圾食品（高热量、高糖和/或高脂肪食品）相关的巴甫洛夫条件刺激，比如布朗尼蛋糕的香味，会引发进食欲望并增加食物摄入量。更容易受到这些食物线索动机性影响的人可能有更高的肥胖风险。此外，过量食用垃圾食品导致肥胖的发展本身可能会增强对食物线索的吸引力。在这里，我们使用了一个对垃圾食品饮食诱导肥胖敏感的个体模型，来确定对蔗糖配对线索的吸引力和动机是否存在预先存在的和/或饮食诱导的增加（即动机显著性或“渴望”）。我们还评估了中脑边缘功能和受体表达在饮食与肥胖相关方面的变化。我们发现，易患饮食诱导肥胖的大鼠在肥胖发展之前就表现出增强的条件性趋近行为。此外，在接触垃圾食品饮食后，那些肥胖的大鼠也表现出更愿意获取蔗糖线索。增强的“渴望”并非由于蔗糖享乐影响（“喜好”）的个体差异。从神经生物学角度来看，μ阿片受体mRNA表达在纹状体“热点”区域较低，而这些区域仅在那些肥胖的大鼠中产生进食或享乐影响。相比之下，长期接触垃圾食品导致对苯丙胺诱导的运动产生交叉敏感，并导致纹状体D2R mRNA下调，无论是否发生肥胖。这些数据共同揭示了接触垃圾食品饮食的行为和神经生物学后果中的个体差异，以及易感个体中动机致敏对更大的食物线索触发动机的潜在贡献。
