ArticleNeurobiology of disease2013
Role of glutamic acid decarboxylase 67 in regulating cortical parvalbumin and GABA membrane transporter 1 expression: implications for schizophrenia.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- Can Sodium Oxybate Mitigate the Symptoms of Schizophrenia?Current neuropharmacology · 2026Review
- Exploration of schizophrenia-related behavioral and molecular abnormalities in a mutant mouse model with a mutation in the TVV motif of the ErbB4 gene.Molecular brain · 2025Article
- The Pathophysiological Underpinnings of Gamma-Band Alterations in Psychiatric Disorders.Life (Basel, Switzerland) · 2024Review
- Schizophrenia in the genetic era: a review from development history, clinical features and genomic research approaches to insights of susceptibility genes.Metabolic brain disease · 2024Review
- Disclosing common biological signatures and predicting new therapeutic targets in schizophrenia and obsessive-compulsive disorder by integrated bioinformatics analysis.BMC psychiatry · 2023Article
- Tonic activation of GABAFrontiers in synaptic neuroscience · 2023Article
- Beyond the γ-aminobutyric acid hypothesis of schizophrenia.Frontiers in cellular neuroscience · 2023Review
- KCNH2-3.1 mediates aberrant complement activation and impaired hippocampal-medial prefrontal circuitry associated with working memory deficits.Molecular psychiatry · 2020Article
- Alterations in cortical interneurons and cognitive function in schizophrenia.Neurobiology of disease · 2019Review
- Correlations of Post-stroke Depression with Inflammatory Response Factors.Iranian journal of public health · 2018Article
- MiR-200c-3p inhibits cell migration and invasion of clear cell renal cell carcinoma via regulating SLC6A1.Cancer biology & therapy · 2018Article
- Gastrodin Rescues Autistic-Like Phenotypes in Valproic Acid-Induced Animal Model.Frontiers in neurology · 2018Article
- Decreasing GABA function within the medial prefrontal cortex or basolateral amygdala decreases sociability.Behavioural brain research · 2017Article
- Cortical Gene Expression After a Conditional Knockout of 67 kDa Glutamic Acid Decarboxylase in Parvalbumin Neurons.Schizophrenia bulletin · 2016Article
- Genetic deletion of fibroblast growth factor 14 recapitulates phenotypic alterations underlying cognitive impairment associated with schizophrenia.Translational psychiatry · 2016Article
- Targeting Prefrontal Cortical Systems for Drug Development: Potential Therapies for Cognitive Disorders.Annual review of pharmacology and toxicology · 2016Review
- Interneuron epigenomes during the critical period of cortical plasticity: Implications for schizophrenia.Neurobiology of learning and memory · 2015Review
- Effects of chronic inhibition of GABA synthesis on attention and impulse control.Pharmacology, biochemistry, and behavior · 2015Article
- Review
- GABAergic control of depression-related brain states.Advances in pharmacology (San Diego, Calif.) · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Markers of GABA neurotransmission are altered in multiple regions of the neocortex in individuals with schizophrenia. Lower levels of glutamic acid decarboxylase 67 (GAD67) mRNA and protein, which is responsible for most cortical GABA synthesis, are accompanied by lower levels of GABA membrane transporter 1 (GAT1) mRNA. These alterations are thought to be most prominent in the parvalbumin (PV)-containing subclass of interneurons, which also contain lower levels of PV mRNA. Since GAT1 and PV each reduce the availability of GABA at postsynaptic receptors, lower levels of GAT1 and PV mRNAs have been hypothesized to represent compensatory responses to an upstream reduction in cortical GABA synthesis in schizophrenia. However, such cause-and-effect hypotheses cannot be directly tested in a human illness. Consequently, we used two mouse models with reduced GAD67 expression specifically in PV neurons (PV(GAD67+/-)) or in all interneurons (GABA(GAD67+/-)) and quantified GAD67, GAT1 and PV mRNA levels using methods identical to those employed in studies of schizophrenia. Cortical levels of PV or GAT1 mRNAs were not altered in PV(GAD67+/-) mice during postnatal development or in adulthood. Furthermore, cellular analyses confirmed the predicted reduction in GAD67 mRNA, but failed to show a deficit in PV mRNA in these animals. Levels of PV and GAT1 mRNAs were also unaltered in GABA(GAD67+/-) mice. Thus, mouse lines with cortical reductions in GAD67 mRNA that match or exceed those present in schizophrenia, and that differ in the developmental timing and cell type-specificity of the GAD67 deficit, failed to provide proof-of-concept evidence that lower PV and GAT1 expression in schizophrenia are a consequence of lower GAD67 expression. Together, these findings suggest that the correlated decrements in cortical GAD67, PV and GAT1 mRNAs in schizophrenia may be a common consequence of some other upstream factor.
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