GIT1 is associated with ADHD in humans and ADHD-like behaviors in mice
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.
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Elevated E/I ratio has been implicated in the neuropathology of other psychiatric disorders, including autism spectrum disorders and attention-deficit/hyperactivity disorder, both of which exhibit working memory deficits.
“Elevated E/I ratio has been implicated in the neuropathology of other psychiatric disorders, including autism spectrum disorders (Rubenstein and Merzenich 2003;Yizhar et al. 2011) and attention-deficit/hyperactivity disorder (Won et al. 2011), both of which exhibit WM deficits (Martinussen et al. 2005;Williams et al. 2005).”
From Linking microcircuit dysfunction to cognitive impairment: Effects of disinhibition associated with schizophrenia in a cortical working memory model (2014) · cites this paper as Won et al. 2011
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- Authors
- Won, H., Mah, W., Kim, E., Kim, J.-W., Hahm, E.-K., Kim, M.-H., Cho, S., Kim, J., Jang, H., Cho, S.-C., Kim, B.-N., Shin, M.-S., Seo, J., Jeong, J., Choi, S.-Y., Kim, D., Kang, C., & Kim, E.
- Affiliations
- Korea Advanced Institute of Science and Technology (KR)
- Seoul National University (KR)
- Corresponding author
- Kang, Changwon
- Kim, Eunjoon
- ORCID
- Venue
- Nature Medicine
- Published
- 2011-04-17
- Volume
- 17
- Issue
- 5
- Pages
- 566-572
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2106846323
- Cited by
- 156
- References
- 62
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 6 · 2023: 9 · 2022: 10 · 2021: 9 · 2020: 15 · 2019: 5 · 2018: 13 · 2017: 7 · 2016: 11 · 2015: 13 · 2014: 11 · 2013: 10 · 2012: 13
- FWCI
- 8.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Seoul National University Open Repository (Seoul National University) (submittedVersion)
- Funders
- National Research Foundation of Korea
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- GIT1, attention deficit hyperactivity disorder, single nucleotide polymorphisms, genetic susceptibility, hyperactivity, learning and memory impairment, EEG theta rhythm, psychostimulants, amphetamine, methylphenidate, Rac1 signaling, presynaptic inhibition, excitation-inhibition balance
- MeSH terms
- Amphetamine, Central Nervous System Stimulants, Animals, Attention Deficit Disorder with Hyperactivity, Brain, Child, Disease Models, Animal, Electroencephalography, Female, Humans, Male, Memory Disorders, Methylphenidate, Motor Activity, Synaptic Transmission, Neuropeptides, Phenotype, Signal Transduction, Mice, Knockout, Cell Cycle Proteins, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, GTPase-Activating Proteins, rac GTP-Binding Proteins, rac1 GTP-Binding Protein, Adaptor Proteins, Signal Transducing, Mice
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