ArticleExperimental neurobiology2017
Decreased Glial GABA and Tonic Inhibition in Cerebellum of Mouse Model for Attention-Deficit/Hyperactivity Disorder (ADHD).
Article in Experimental neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- Modelling synaptic dysfunction in childhood dementia using human iPSC-derived cortical networks.Nature communications · 2026Article
- Aniracetam restores the excitation-inhibition balance of neurotransmitters in the prefrontal cortex of mice with ADHD.Scientific reports · 2026Article
- Suppressing astrocytic GABA transaminase enhances tonic inhibition and weakens hippocampal spatial memory.Experimental & molecular medicine · 2025Article
- Neuronal cell type specific roles for Nprl2 in neurodevelopmental disorder-relevant behaviors.Neurobiology of disease · 2025Article
- Association between genetic polymorphisms of synaptophysin (SYP) gene and attention deficit hyperactivity disorder in Korean subjects.Genes & genomics · 2023Article
- GABA tone regulation and its cognitive functions in the brain.Nature reviews. Neuroscience · 2023Review
- Sex and Age-Dependent Olfactory Memory Dysfunction in ADHD Model Mice.Life (Basel, Switzerland) · 2023Article
- Improved gliotransmission by increasing intracellular CaJournal of nanobiotechnology · 2022Article
- Inhibiting peripheral and central MAO-B ameliorates joint inflammation and cognitive impairment in rheumatoid arthritis.Experimental & molecular medicine · 2022Article
- Generation of Astrocyte-Specific MAOB Conditional Knockout Mouse with Minimal Tonic GABA Inhibition.Experimental neurobiology · 2022Article
- Neurochemistry of Visual Attention.Frontiers in neuroscience · 2021Review
- Astrocyte Role in Temporal Lobe Epilepsy and Development of Mossy Fiber Sprouting.Frontiers in cellular neuroscience · 2021Review
- Critical Role of Astrocytic Polyamine and GABA Metabolism in Epileptogenesis.Frontiers in cellular neuroscience · 2021Article
- Cerebellum-Specific Deletion of the GABACell reports · 2020Article
- Biomarker discovery in attention deficit hyperactivity disorder: RNA sequencing of whole blood in discordant twin and case-controlled cohorts.BMC medical genomics · 2020Article
- Amyloidosis is associated with thicker myelin and increased oligodendrogenesis in the adult mouse brain.Journal of neuroscience research · 2020Article
- Review
- Neurofibromatosis Type 1 Implicates Ras Pathways in the Genetic Architecture of Neurodevelopmental Disorders.Behavior genetics · 2020Review
- Glial Factors Regulating White Matter Development and Pathologies of the Cerebellum.Neurochemical research · 2020Review
- Neuroprotective Effect of CatalpolFrontiers in pharmacology · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
About 5~12% of school-aged children suffer from the Attention-Deficit/Hyperactivity Disorder (ADHD). However, the core mechanism of ADHD remains unclear. G protein-coupled receptor kinase-interacting protein-1 (GIT1) has recently been reported to be associated with ADHD in human and the genetic deletion of GIT1 result in ADHD-like behaviors in mice. Mice lacking GIT1 shows a shift in neuronal excitation/inhibition (E/I) balance. However, the pricise mechanism for E/I imbalance and the role of neuron-glia interaction in GIT1 knockout (KO) mice have not been studied. Especially, a possible contribution of glial GABA and tonic inhibition mediated by astrocytic GABA release in the mouse model for ADHD remains unexplored. Therefore, we investigated the changes in the amount of GABA and degree of tonic inhibition in GIT1 KO mice. We observed a decreased glial GABA intensity in GIT1 KO mice compared to wild type (WT) mice and an attenuation of tonic current from cerebellar granule cells in GIT1 KO mice. Our study identifies the previously unknown mechanism of reduced astrocytic GABA and tonic inhibition in GIT1 lacking mice as a potential cause of hyperactivity disorder.
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