ArticleNature neuroscience2018
Restoring wild-type-like CA1 network dynamics and behavior during adulthood in a mouse model of schizophrenia.
Article in Nature neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Hippocampal transcriptome profiling in a 22q11.2 deletion syndrome mouse model: comparison with human schizophrenia.Molecular brain · 2026Article
- Disorganized Inhibitory Dynamics in Hippocampal area CA1 of 22q11.2 Deletion Mutant Mice.bioRxiv : the preprint server for biology · 2026Article
- Cognitive impairment following maternal separation in rats mediated by the NADTranslational psychiatry · 2025Article
- Parvalbumin interneurons: the dark and bright sides of a key playmaker of neural circuits and behavior.Frontiers in cellular neuroscience · 2025Review
- Identifying dysfunctional cell types and circuits in animal models for psychiatric disorders with calcium imaging.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Gamma oscillation plasticity is mediated via parvalbumin interneurons.Science advances · 2024Article
- Neurobiology of schizophrenia.Current opinion in neurobiology · 2024Review
- Mechanisms of copy number variants in neuropsychiatric disorders: From genes to therapeutics.Current opinion in neurobiology · 2023Review
- Article
- Article
- Pharmacogenetic activation of parvalbumin interneurons in the prefrontal cortex rescues cognitive deficits induced by adolescent MK801 administration.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Control of sustained attention and impulsivity by GTranslational psychiatry · 2023Article
- Pathological oligodendrocyte precursor cells revealed in human schizophrenic brains and trigger schizophrenia-like behaviors and synaptic defects in genetic animal model.Molecular psychiatry · 2022Article
- Reduced expression of the psychiatric risk gene DLG2 (PSD93) impairs hippocampal synaptic integration and plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Synaptic Plasticity Dysfunctions in the Pathophysiology of 22q11 Deletion Syndrome: Is There a Role for Astrocytes?International journal of molecular sciences · 2022Review
- Cell type-specific mechanism of Setd1a heterozygosity in schizophrenia pathogenesis.Science advances · 2022Article
- Chemogenetics as a neuromodulatory approach to treating neuropsychiatric diseases and disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency.eLife · 2022Article
- Sparser and Less Efficient Hippocampal-Prefrontal Projections account for Developmental Network Dysfunction in a Model of Psychiatric Risk Mediated by Gene-Environment Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schizophrenia is a severely debilitating neurodevelopmental disorder. Establishing a causal link between circuit dysfunction and particular behavioral traits that are relevant to schizophrenia is crucial to shed new light on the mechanisms underlying the pathology. We studied an animal model of the human 22q11 deletion syndrome, the mutation that represents the highest genetic risk of developing schizophrenia. We observed a desynchronization of hippocampal neuronal assemblies that resulted from parvalbumin interneuron hypoexcitability. Rescuing parvalbumin interneuron excitability with pharmacological or chemogenetic approaches was sufficient to restore wild-type-like CA1 network dynamics and hippocampal-dependent behavior during adulthood. In conclusion, our data provide insights into the network dysfunction underlying schizophrenia and highlight the use of reverse engineering to restore physiological and behavioral phenotypes in an animal model of neurodevelopmental disorder.
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