Enhanced appetitive learning and reversal learning in a mouse model for Prader-Willi syndrome.
Enhanced appetitive learning and reversal learning in a mouse model for Prader-Willi syndrome.
复制标题
增强普瑞德威利综合征小鼠模型的食欲学习和逆转学习。
作者：
Dinko Relkovic;T. Humby;J. Hagan;L. Wilkinson;A. Isles
Prader-Willi综合征（PWS）是由于人类染色体15 q11-q13上的印记基因簇缺乏父系来源的基因表达而引起的。PWS的特征是严重的肌张力减退，婴儿期无法茁壮成长，并且在婴儿期出现时，由于异常的饱腹反应和食物增加的动力而出现学习障碍和暴饮暴食行为的证据。我们之前已经表明，一个印记中心缺失小鼠模型（PWS-IC）更快地获得偏好，并消耗更多的美味食物。在这里，我们研究了如何使用这种可口的食物作为一个开胃菜的影响PWS-IC小鼠进行一个简单的食欲学习任务的学习。在非空间迷宫任务中，PWS-IC小鼠获得标准的速度要快得多，在初始获取和反向学习过程中错误更少。一个操纵，其中的免疫球蛋白是贬值损害野生型的性能，但没有影响PWS-IC小鼠。这表明，PWS-IC小鼠对学习者的动机增加可能是其增强学习的基础。这支持了以前在PWS患者中的发现，并且是第一个PWS动物模型的行为研究，其中食物奖励的行为动机已经被检查。
Prader-Willi syndrome (PWS) is caused by lack of paternally derived gene expression from the imprinted gene cluster on human chromosome 15q11-q13. PWS is characterized by severe hypotonia, a failure to thrive in infancy and, on emerging from infancy, evidence of learning disabilities and overeating behavior due to an abnormal satiety response and increased motivation by food. We have previously shown that an imprinting center deletion mouse model (PWS-IC) is quicker to acquire a preference for, and consume more of a palatable food. Here we examined how the use of this palatable food as a reinforcer influences learning in PWS-IC mice performing a simple appetitive learning task. On a nonspatial maze-based task, PWS-IC mice acquired criteria much quicker, making fewer errors during initial acquisition and also reversal learning. A manipulation where the reinforcer was devalued impaired wild-type performance but had no effect on PWS-IC mice. This suggests that increased motivation for the reinforcer in PWS-IC mice may underlie their enhanced learning. This supports previous findings in PWS patients and is the first behavioral study of an animal model of PWS in which the motivation of behavior by food rewards has been examined.