ArticleAttention deficit and hyperactivity disorders2018
Hyperactivity in mice lacking one allele of the glutamic acid decarboxylase 67 gene.
Article in Attention deficit and hyperactivity disorders, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Aberrant glutamatergic systems underlying impulsive behaviors: Insights from clinical and preclinical research.Progress in neuro-psychopharmacology & biological psychiatry · 2024Review
- Effects of Environmental Noise Stress on Mouse Metabolism.International journal of molecular sciences · 2024Article
- Transplantation of neural stem progenitor cells from different sources for severe spinal cord injury repair in rat.Bioactive materials · 2023Article
- Investigating the Role of GABA in Neural Development and Disease Using Mice Lacking GAD67 or VGAT Genes.International journal of molecular sciences · 2022Review
- Global knockdown of glutamate decarboxylase 67 elicits emotional abnormality in mice.Molecular brain · 2021Article
- Vascular amyloid accumulation alters the gabaergic synapse and induces hyperactivity in a model of cerebral amyloid angiopathy.Aging cell · 2020Article
- Glutamic acid decarboxylase 67 haplodeficiency in mice: consequences of postweaning social isolation on behavior and changes in brain neurochemical systems.Brain structure & function · 2020Article
- Neuroinflammation as a risk factor for attention deficit hyperactivity disorder.Pharmacology, biochemistry, and behavior · 2019Review
- Genetic polymorphism and neuroanatomical changes in schizophrenia.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
GABAergic interneuron loss, maturational delay or imbalance of glutamatergic to GABAergic signaling has been implicated in several neuropsychiatric disorders including Tourette syndrome and attention-deficit/hyperactivity disorder (ADHD). In schizophrenia, decreases in parvalbumin (PV), somatostatin (Sst) and glutamic acid decarboxylase (GAD) RNA have been observed and seem to indicate a failure in maturation in PV and Sst neurons. In Tourette syndrome, which has a high level of comorbid ADHD, reduced numbers of parvalbumin expressing neurons have been observed in the basal ganglia of affected patients. In addition, polymorphisms in the GAD1 gene that codes for GAD67 protein have been associated with ADHD. We have examined whether mice with a disrupted Gad67 allele, the Gad67 GFP knock-in mice (Gad67-GFP
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.