抄録
Attention-deficit/hyperactivity disorder (ADHD) is a common neuropsychiatric disorder in children. Although animal models and human brain imaging studies indicate a significant role for glutamatergic dysfunction in ADHD, there is no direct evidence that glutamatergic dysfunction is sufficient to induce ADHD-like symptoms. The glial glutamate transporter GLT1 plays a critical role in glutamatergic neurotransmission. We report here the generation of mice expressing only 20% of normal levels of the GLT1. Unlike conventional GLT1 knockout mice, these mice survive to adulthood and exhibit ADHD-like phenotypes, including hyperactivity, impulsivity and impaired memory. These findings indicate that glutamatergic dysfunction due to GLT1 deficiency, a mechanism distinct from the dopaminergic deficit hypothesis of ADHD, underlies ADHD-like symptoms.
本文言語 | English |
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ページ(範囲) | 161-165 |
ページ数 | 5 |
ジャーナル | Biochemical and Biophysical Research Communications |
巻 | 567 |
DOI | |
出版ステータス | Published - 2021 8月 27 |
ASJC Scopus subject areas
- 生物理学
- 生化学
- 分子生物学
- 細胞生物学