ArticleSchizophrenia bulletin2014
Cortical inhibitory neuron disturbances in schizophrenia: role of the ontogenetic transcription factor Lhx6.
Article in Schizophrenia bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Transcription Factors in the Pathogenesis of Schizophrenia.Life (Basel, Switzerland) · 2026Review
- Genome-wide association and DNA methylation analyses of SSRI treatment response in major depressive disorder.BMC psychiatry · 2025Article
- Mediation of DNA methylation (cg04622888 and cg05037505) in the association between childhood maltreatment and non-suicidal self-injury in early adolescents.European child & adolescent psychiatry · 2025Article
- Gene, cell type, and drug prioritization analysis suggest genetic basis for the utility of diuretics in treating Alzheimer disease.HGG advances · 2023Article
- Genetic Regulation of Vertebrate Forebrain Development by Homeobox Genes.Frontiers in neuroscience · 2022Review
- Development, Diversity, and Death of MGE-Derived Cortical Interneurons.International journal of molecular sciences · 2021Review
- Involvement of the nuclear factor-κB transcriptional complex in prefrontal cortex immune activation in bipolar disorder.Translational psychiatry · 2021Article
- Developmental alterations in the transcriptome of three distinct rodent models of schizophrenia.PloS one · 2020Article
- White matter neuron biology and neuropathology in schizophrenia.NPJ schizophrenia · 2019Review
- CTCF Governs the Identity and Migration of MGE-Derived Cortical Interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The Role of the Nuclear Factor-κB Transcriptional Complex in Cortical Immune Activation in Schizophrenia.Biological psychiatry · 2019Article
- Role of microglia disturbances and immune-related marker abnormalities in cortical circuitry dysfunction in schizophrenia.Neurobiology of disease · 2017Review
- Altered expression of developmental regulators of parvalbumin and somatostatin neurons in the prefrontal cortex in schizophrenia.Schizophrenia research · 2016Article
- Cortical GABA markers identify a molecular subtype of psychotic and bipolar disorders.Psychological medicine · 2016Article
- The Role of Endocannabinoid Signaling in Cortical Inhibitory Neuron Dysfunction in Schizophrenia.Biological psychiatry · 2016Review
- A Role for the Transcription Factor Nk2 Homeobox 1 in Schizophrenia: Convergent Evidence from Animal and Human Studies.Frontiers in behavioral neuroscience · 2016Article
- Molecular mechanisms and timing of cortical immune activation in schizophrenia.The American journal of psychiatry · 2015Article
- Interneuron epigenomes during the critical period of cortical plasticity: Implications for schizophrenia.Neurobiology of learning and memory · 2015Review
- Chemokine receptors and cortical interneuron dysfunction in schizophrenia.Schizophrenia research · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Disturbances in parvalbumin- and somatostatin-containing neurons, including deficits in the gamma-aminobutyric acid (GABA)-synthesizing enzyme GAD67 in the prefrontal cortex (PFC) in schizophrenia, may be related to disrupted pre- and/or postnatal development. Deficits in the transcription factor Lhx6, which regulates parvalbumin and somatostatin neuron development, are associated with GAD67 deficits in schizophrenia. Therefore, we investigated the potential pre- and postnatal roles of Lhx6 in GABA-related disturbances using qPCR and/or in situ hybridization to quantify PFC levels of (1) Lhx6 mRNA in a new cohort of schizophrenia subjects; (2) Lhx6 mRNA in monkeys across postnatal development; (3) GABA-related mRNAs in Lhx6 heterozygous (Lhx6+/−) mice, which model Lhx6 deficits in schizophrenia; and (4) Lhx6 mRNA in GAD67+/− mice, which model GAD67 deficits in schizophrenia. Lhx6 mRNA levels were lower (−15%) in schizophrenia and correlated with lower GAD67 mRNA levels. In addition, Lhx6 mRNA levels declined 24% from the perinatal to prepubertal periods then stabilized in monkeys. Finally, GAD67, parvalbumin, and somatostatin mRNAs were not altered in Lhx6+/− mice, and Lhx6 mRNA was not altered in GAD67+/− mice. These data suggest that PFC Lhx6 and GAD67 mRNA deficits are common components of GABA neuron pathology in schizophrenia. An excessive early postnatal decline in Lhx6 mRNA might contribute to Lhx6 mRNA deficits in schizophrenia. However, a partial loss of Lhx6 is not sufficient in isolation to produce deficits in GAD67 mRNA and vice versa, suggesting that the concurrence of Lhx6 and GAD67 mRNA deficits in schizophrenia may instead be the consequence of a common upstream factor.
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