ArticleScientific reports2017
Chrna7 deficient mice manifest no consistent neuropsychiatric and behavioral phenotypes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 66 citations in OpenAlex.
- Establishment and Characterization of a Brain-Derived Cell Line from Japanese Eel (Animals : an open access journal from MDPI · 2026Article
- Astrocytes mediate the pro-cognitive value of α7nAChRs and of α7nAChR-targeting therapeutics.bioRxiv : the preprint server for biology · 2026Article
- Therapeutic Targeting of the α7 Nicotinic Receptor: Challenges and Prospects for Cognitive Improvement in Alzheimer's and Schizophrenia.Basic & clinical pharmacology & toxicology · 2025Review
- A Paradigmatic Case of Genetic Overlap Between Neurodevelopment Disorders and Schizophrenia Aligning with the Neurodevelopmental Continuum Hypothesis.International journal of molecular sciences · 2025Article
- Impaired OTUD7A-dependent Ankyrin regulation mediates neuronal dysfunction in mouse and human models of the 15q13.3 microdeletion syndrome.Molecular psychiatry · 2023Article
- Genetic deletion of α7 nAChRs reduces hippocampal granule and pyramidal cell number in both sexes but impairs pattern separation in males only.Frontiers in neuroscience · 2023Article
- Loss of function of OTUD7A in the schizophrenia- associated 15q13.3 deletion impairs synapse development and function in human neurons.American journal of human genetics · 2022Article
- α7 nicotinic acetylcholine receptors in the hippocampal circuit: taming complexity.Trends in neurosciences · 2022Review
- Deepening the understanding of CNVs on chromosome 15q11-13 by using hiPSCs: An overview.Frontiers in cell and developmental biology · 2022Review
- Altered neuronal physiology, development, and function associated with a common chromosome 15 duplication involving CHRNA7.BMC biology · 2021Article
- Article
- Dissecting the complexity of CNV pathogenicity: insights from Drosophila and zebrafish models.Current opinion in genetics & development · 2021Review
- Mice with mutations in Trpm1, a gene in the locus of 15q13.3 microdeletion syndrome, display pronounced hyperactivity and decreased anxiety-like behavior.Molecular brain · 2021Article
- Nicotinic Receptors in Sleep-Related Hypermotor Epilepsy: Pathophysiology and Pharmacology.Brain sciences · 2020Review
- α7 nicotinic acetylcholine receptors as therapeutic targets in schizophrenia: Update on animal and clinical studies and strategies for the future.Neuropharmacology · 2020Review
- Regulation of aggressive behaviors by nicotinic acetylcholine receptors: Animal models, human genetics, and clinical studies.Neuropharmacology · 2020Review
- A Link between Genetic Disorders and Cellular Impairment, Using Human Induced Pluripotent Stem Cells to Reveal the Functional Consequences of Copy Number Variations in the Central Nervous System-A Close Look at Chromosome 15.International journal of molecular sciences · 2020Review
- First report of two successive deletions on chromosome 15q13 cytogenetic bands in a boy and girl: additional data to 15q13.3 syndrome with a report of high IQ patient.Molecular cytogenetics · 2019Article
- An interaction-based model for neuropsychiatric features of copy-number variants.PLoS genetics · 2019Article
- Proteomic Investigation of Murine Neuronal α7-Nicotinic Acetylcholine Receptor Interacting Proteins.Journal of proteome research · 2018Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The alpha7 nicotinic acetylcholine receptor, encoded by the CHRNA7 gene, has been implicated in various psychiatric and behavioral disorders, including schizophrenia, bipolar disorder, epilepsy, autism, Alzheimer's disease, and Parkinson's disease, and is considered a potential target for therapeutic intervention. 15q13.3 microdeletion syndrome is a rare genetic disorder, caused by submicroscopic deletions on chromosome 15q. CHRNA7 is the only gene in this locus that has been deleted entirely in cases involving the smallest microdeletions. Affected individuals manifest variable neurological and behavioral phenotypes, which commonly include developmental delay/intellectual disability, epilepsy, and autism spectrum disorder. Subsets of patients have short attention spans, aggressive behaviors, mood disorders, or schizophrenia. Previous behavioral studies suggested that Chrna7 deficient mice had attention deficits, but were normal in baseline behavioral responses, learning, memory, and sensorimotor gating. Given a growing interest in CHRNA7-related diseases and a better appreciation of its associated human phenotypes, an in-depth behavioral characterization of the Chrna7 deficient mouse model appeared prudent. This study was designed to investigate whether Chrna7 deficient mice manifest phenotypes related to those seen in human individuals, using an array of 12 behavioral assessments and electroencephalogram (EEG) recordings on freely-moving mice. Examined phenotypes included social interaction, compulsive behaviors, aggression, hyperactivity, anxiety, depression, and somatosensory gating. Our data suggests that mouse behavior and EEG recordings are not sensitive to decreased Chrna7 copy number.
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