Gamma aminobutyric acid transporter subtype 1 gene knockout mice： a new model for attention deficit/hyperactivity disorder

• Published in: Acta biochimica et biophysica Sinica 2013-07, Vol.45 (7), p.578-585
• Main Authors: Yang, Ping, Cai, Guoqiang, Cai, Youqing, Fei, Jian, Liu, Guoxiang
• Format: Article
• Language: English
• Subjects: Animals; Attention Deficit Disorder with Hyperactivity - genetics; Behavior, Animal; Disease Models, Animal; GABA Plasma Membrane Transport Proteins - genetics; GAT1; Male; Mice; Mice, Knockout; Morris水迷宫; γ-氨基丁酸转运蛋白; 亚型; 基因敲除; 小鼠; 注意力; 缺陷
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmt043

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.