ArticleScientific reports2016
Akting up in the GABA hypothesis of schizophrenia: Akt1 deficiency modulates GABAergic functions and hippocampus-dependent functions.
Article in Scientific reports, 2016. 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, 25 citations in OpenAlex.
- Circulating microRNA molecular signatures converge with erythroid phenotypes and iron homeostasis in pediatric tic disorders.Frontiers in psychiatry · 2026Article
- The role of dorsomedial striatum and parvalbumin interneurons in schizophrenia-related cognitive deficits: insights from disrupted strategic decision-making in Akt1 heterozygous mice.Translational psychiatry · 2025Article
- Integrative metabolomics-genomics analysis identifies key networks in a stem cell-based model of schizophrenia.Molecular psychiatry · 2024Article
- Differential effects of AKT1 and AKT2 on sleep-wake activity under basal conditions and in response to LPS challenge in mice.Sleep and biological rhythms · 2024Article
- Neurostructural changes in schizophrenia and treatment-resistance: a narrative review.Psychoradiology · 2024Review
- Bibliometric Analysis on GABA-A Receptors Research Based on CiteSpace and VOSviewer.Journal of pain research · 2023Article
- Network Biology Approaches to Uncover Therapeutic Targets Associated with Molecular Signaling Pathways from circRNA in Postoperative Cognitive Dysfunction Pathogenesis.Journal of molecular neuroscience : MN · 2022Article
- Identification of Peripheral Blood miRNA Biomarkers in First-Episode Drug-Free Schizophrenia Patients Using Bioinformatics Strategy.Molecular neurobiology · 2022Article
- Computer-Aided Drug Design (CADD) to De-Orphanize Marine Molecules: Finding Potential Therapeutic Agents for Neurodegenerative and Cardiovascular Diseases.Marine drugs · 2022Article
- PKBβ/AKT2 deficiency impacts brain mTOR signaling, prefrontal cortical physiology, hippocampal plasticity and select murine behaviors.Molecular psychiatry · 2021Article
- Review
- High Mobility Group Box 1/Toll-like Receptor 4 Signaling IncreasesNeuropsychiatric disease and treatment · 2021Article
- Immunohistological Examination of AKT Isoforms in the Brain: Cell-Type Specificity That May Underlie AKT's Role in Complex Brain Disorders and Neurological Disease.Cerebral cortex communications · 2021Article
- Article
- Neurodevelopmental concepts of schizophrenia in the genome-wide association era: AKT/mTOR signaling as a pathological mediator of genetic and environmental programming during development.Schizophrenia research · 2020Article
- Lithium for schizophrenia: supporting evidence from a 12-year, nationwide health insurance database and from Akt1-deficient mouse and cellular models.Scientific reports · 2020Article
- Enriched Environment Reverts Somatostatin Interneuron Loss in MK-801 Model of Schizophrenia.Molecular neurobiology · 2020Article
- Toward the Language Oscillogenome.Frontiers in psychology · 2018Article
- Genetic polymorphism and neuroanatomical changes in schizophrenia.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence implies that both AKT1 and GABAA receptor (GABAAR) subunit genes are involved in schizophrenia pathogenesis. Activated Akt promotes GABAergic neuron differentiation and increases GABAAR expression on the plasma membrane. To elucidate the role of Akt1 in modulating GABAergic functions and schizophrenia-related cognitive deficits, a set of 6 in vitro and in vivo experiments was conducted. First, an Akt1/2 inhibitor was applied to evaluate its effect on GABAergic neuron-like cell formation from P19 cells. Inhibiting Akt resulted in a reduction in parvalbumin-positive neuron-like cells. In Akt1(-/-) and wild-type mice, seizures induced using pentylenetetrazol (a GABAAR antagonist) were measured, and GABAAR expression and GABAergic interneuron abundance in the brain were examined. Female Akt1(-/-) mice, but not male Akt1(-/-) mice, exhibited less pentylenetetrazol-induced convulsive activity than their corresponding wild-type controls. Reduced parvalbumin-positive interneuron abundance and GABAAR subunit expression, especially in the hippocampus, were also observed in female Akt1(-/-) mice compared to female wild-type mice. Neuromorphometric analyses revealed significantly reduced neurite complexity in hippocampal pyramidal neurons. Additionally, female Akt1(-/-) mice displayed increased hippocampal oscillation power and impaired spatial memory compared to female wild-type mice. Our findings suggest that Akt1 deficiency modulates GABAergic interneurons and GABAAR expression, contributing to hippocampus-dependent cognitive functional impairment.
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