GIT1 is associated with ADHD in humans and ADHD-like behaviors in mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-05

AUTHORS

Hyejung Won, Won Mah, Eunjin Kim, Jae-Won Kim, Eun-Kyoung Hahm, Myoung-Hwan Kim, Sukhee Cho, Jeongjin Kim, Hyeran Jang, Soo-Churl Cho, Boong-Nyun Kim, Min-Sup Shin, Jinsoo Seo, Jaeseung Jeong, Se-Young Choi, Daesoo Kim, Changwon Kang, Eunjoon Kim

ABSTRACT

Attention deficit hyperactivity disorder (ADHD) is a psychiatric disorder that affects ~5% of school-aged children; however, the mechanisms underlying ADHD remain largely unclear. Here we report a previously unidentified association between G protein-coupled receptor kinase-interacting protein-1 (GIT1) and ADHD in humans. An intronic single-nucleotide polymorphism in GIT1, the minor allele of which causes reduced GIT1 expression, shows a strong association with ADHD susceptibility in humans. Git1-deficient mice show ADHD-like phenotypes, with traits including hyperactivity, enhanced electroencephalogram theta rhythms and impaired learning and memory. Hyperactivity in Git1(-/-) mice is reversed by amphetamine and methylphenidate, psychostimulants commonly used to treat ADHD. In addition, amphetamine normalizes enhanced theta rhythms and impaired memory. GIT1 deficiency in mice leads to decreases in ras-related C3 botulinum toxin substrate-1 (RAC1) signaling and inhibitory presynaptic input; furthermore, it shifts the neuronal excitation-inhibition balance in postsynaptic neurons toward excitation. Our study identifies a previously unknown involvement of GIT1 in human ADHD and shows that GIT1 deficiency in mice causes psychostimulant-responsive ADHD-like phenotypes. More... »

PAGES

566

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm.2330

DOI

http://dx.doi.org/10.1038/nm.2330

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005752591

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21499268


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