注意赤字 / 活动过度混乱(ADHD ) 被活动过度描绘,损害持续注意, impulsivity,并且被改变听说困难和缺乏马达协作的度通常伴随。然而, ADHD 的 pathophysiology 和病原学到目前为止仍然保持不确定。我们的以前的研究证明了 gamma aminobutyric 酸 transporter 子类型 1 (GAT1 ) 基因大美人(ko ) 老鼠(gat1/) 是在莫利斯舞水迷宫的活动过度、展出的损害存储器性能。在当前的学习,我们发现 gat1/ 老鼠显示出注意的集中的底层并且增加了 impulsivity。另外, gat1/ 老鼠显示了缺点在马达协作和平衡技巧描绘的混乱。在 ko 老鼠的活动过度被 methylphenidate 和安基丙苯减少。一起,这些结果建议那只 GAT1 ko 老鼠是为 ADHD 学习的一个新动物模型, GAT1 可以是一个新目标对待 ADHD。
Attention deficit/hyperactivity disorder (ADHD) is charac-terized by hyperactivity, impaired sustained attention, im- pulsivity, and is usually accompanied by varying degrees of learning difficulties and lack of motor coordination. However, the pathophysiology and etiology of ADHD remain inconclusive so far. Our previous studies have demonstrated that the gamma aminobutyric acid transport- er subtype 1 (GAT1) gene knockout (ko) mouse (gatl-/-) is hyperactive and exhibited impaired memory performance in the Morris water maze. In the current study, we found that the gatl-/- mice showed low levels of attentional fo- cusing and increased impulsivity. In addition, the gatl-~- mice displayed ataxia characterized by defects in motor co-ordination and balance skills. The hyperactivity in the ko mice was reduced by both methylphenidate and amphet- amine. Collectively, these results suggest that GAT1 ko mouse is a new animal model for ADHD studying and GAT1 may be a new target to treat ADHD.