ArticleMolecular and cellular neurosciences2014
Cortical parvalbumin GABAergic deficits with α7 nicotinic acetylcholine receptor deletion: implications for schizophrenia.
Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
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- Functional Characterization of Parallel Fiber-Purkinje Cell Synapses in Two Friedreich's Ataxia Mouse Models.Cerebellum (London, England) · 2025Article
- Dampened α7 nAChR activity contributes to audiogenic seizures and hyperactivity in a mouse model of Fragile X Syndrome.bioRxiv : the preprint server for biology · 2024Article
- Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders.Biochemical Society transactions · 2024Review
- Adolescent nicotine exposure promotes adulthood opioid consumption that persists despite adverse consequences and increases the density of insular perineuronal nets.Addiction neuroscience · 2024Article
- Modulation of ventromedial orbitofrontal cortical glutamatergic activity affects the explore-exploit balance and influences value-based decision-making.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Astroglia in Autism Spectrum Disorder.International journal of molecular sciences · 2021Review
- Morphine coordinates SST and PV interneurons in the prelimbic cortex to disinhibit pyramidal neurons and enhance reward.Molecular psychiatry · 2021Article
- Prefrontal α7nAChR Signaling Differentially Modulates Afferent Drive and Trace Fear Conditioning Behavior in Adolescent and Adult Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- A Meta-Analysis of Bioelectric Data in Cancer, Embryogenesis, and Regeneration.Bioelectricity · 2021Article
- Oxidative Stress-Related Mechanisms in Schizophrenia Pathogenesis and New Treatment Perspectives.Oxidative medicine and cellular longevity · 2021Review
- [Establishment of a gp120 transgenic mouse model withNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Analysis of the brain transcriptome in lines of laying hens divergently selected for feather pecking.BMC genomics · 2020Article
- The origin of NMDA receptor hypofunction in schizophrenia.Pharmacology & therapeutics · 2020Review
- Neuronal serine racemase associates with Disrupted-In-Schizophrenia-1 and DISC1 agglomerates: Implications for schizophrenia.Neuroscience letters · 2019Article
- Plasticity in the Working Memory System: Life Span Changes and Response to Injury.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2018Review
- Early VGLUT1-specific parallel fiber synaptic deficits and dysregulated cerebellar circuit in the KIKO mouse model of Friedreich ataxia.Disease models & mechanisms · 2017Article
- Early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in the KIKO mouse model of Friedreich ataxia.Disease models & mechanisms · 2017Article
- Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia.Molecular psychiatry · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Dysfunction of cortical parvalbumin (PV)-containing GABAergic interneurons has been implicated in cognitive deficits of schizophrenia. In humans microdeletion of the CHRNA7 (α7 nicotinic acetylcholine receptor, nAChR) gene is associated with cortical dysfunction in a broad spectrum of neurodevelopmental and neuropsychiatric disorders including schizophrenia while in mice similar deletion causes analogous abnormalities including impaired attention, working-memory and learning. However, the pathophysiological roles of α7 nAChRs in cortical PV GABAergic development remain largely uncharacterized. In both in vivo and in vitro models, we identify here that deletion of the α7 nAChR gene in mice impairs cortical PV GABAergic development and recapitulates many of the characteristic neurochemical deficits in PV-positive GABAergic interneurons found in schizophrenia. α7 nAChR null mice had decreased cortical levels of GABAergic markers including PV, glutamic acid decarboxylase 65/67 (GAD65/67) and the α1 subunit of GABAA receptors, particularly reductions of PV and GAD67 levels in cortical PV-positive interneurons during late postnatal life and adulthood. Cortical GABAergic synaptic deficits were identified in the prefrontal cortex of α7 nAChR null mice and α7 nAChR null cortical cultures. Similar disruptions in development of PV-positive GABAergic interneurons and perisomatic synapses were found in cortical cultures lacking α7 nAChRs. Moreover, NMDA receptor expression was reduced in GABAergic interneurons, implicating NMDA receptor hypofunction in GABAergic deficits in α7 nAChR null mice. Our findings thus demonstrate impaired cortical PV GABAergic development and multiple characteristic neurochemical deficits reminiscent of schizophrenia in cortical PV-positive interneurons in α7 nAChR gene deletion models. This implicates crucial roles of α7 nAChRs in cortical PV GABAergic development and dysfunction in schizophrenia and other neuropsychiatric disorders.
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