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Gamma aminobutyric acid transporter subtype 1 gene knockout mice: a new model for attention deficit/hyperactivity disorder
Author(s) -
Ping Yang,
Guoqiang Cai,
Youqing Cai,
Jian Fei,
Guoxiang Liu
Publication year - 2013
Publication title -
acta biochimica et biophysica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.771
H-Index - 57
eISSN - 1745-7270
pISSN - 1672-9145
DOI - 10.1093/abbs/gmt043
Subject(s) - impulsivity , methylphenidate , motor coordination , amphetamine , attention deficit hyperactivity disorder , gene knockout , knockout mouse , neurodevelopmental disorder , gamma aminobutyric acid , ataxia , morris water navigation task , neuroscience , psychology , medicine , pharmacology , psychiatry , biology , gene , dopamine , cognition , genetics , receptor , autism
Attention deficit/hyperactivity disorder (ADHD) is characterized by hyperactivity, impaired sustained attention, impulsivity, 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 transporter subtype 1 (GAT1) gene knockout (ko) mouse (gat1-/-) is hyperactive and exhibited impaired memory performance in the Morris water maze. In the current study, we found that the gat1-/- mice showed low levels of attentional focusing and increased impulsivity. In addition, the gat1-/- mice displayed ataxia characterized by defects in motor coordination and balance skills. The hyperactivity in the ko mice was reduced by both methylphenidate and amphetamine. 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.

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