ArticlePloS one2013
Contribution of NMDA receptor hypofunction in prefrontal and cortical excitatory neurons to schizophrenia-like phenotypes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Autism Spectrum Disorder: Focus on Glutamatergic Neurotransmission.International journal of molecular sciences · 2022Review
- Consequences of NMDA receptor deficiency can be rescued in the adult brain.Molecular psychiatry · 2021Article
- Delayed-matching-to-position working memory in mice relies on NMDA-receptors in prefrontal pyramidal cells.Scientific reports · 2021Article
- Article
- Chronic adolescent exposure to ∆9-tetrahydrocannabinol decreases NMDA current and extrasynaptic plasmalemmal density of NMDA GluN1 subunits in the prelimbic cortex of adult male mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Schizophrenia-Like Dopamine Release Abnormalities in a Mouse Model of NMDA Receptor Hypofunction.Schizophrenia bulletin · 2019Article
- Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?Frontiers in psychiatry · 2019Review
- Attenuation Effects of Alpha-Pinene Inhalation on Mice with Dizocilpine-Induced Psychiatric-Like Behaviour.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- NMDAR Hypofunction Animal Models of Schizophrenia.Frontiers in molecular neuroscience · 2019Review
- NMDA-receptor inhibition and oxidative stress during hippocampal maturation differentially alter parvalbumin expression and gamma-band activity.Scientific reports · 2018Article
- Increased cortical neuronal responses to NMDA and improved attentional set-shifting performance in rats following prebiotic (B-GOSEuropean neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2018Article
- Immediate Early Genes Anchor a Biological Pathway of Proteins Required for Memory Formation, Long-Term Depression and Risk for Schizophrenia.Frontiers in behavioral neuroscience · 2018Article
- Ketamine Self-Administration Reduces the Homeostasis of the Glutamate Synapse in the Rat Brain.Molecular neurobiology · 2017Article
- Glutamatergic regulation of cognition and functional brain connectivity: insights from pharmacological, genetic and translational schizophrenia research.British journal of pharmacology · 2017Review
- Single-cell methylomes identify neuronal subtypes and regulatory elements in mammalian cortex.Science (New York, N.Y.) · 2017Article
- Phencyclidine administration during neurodevelopment alters network activity in prefrontal cortex and hippocampus in adult rats.Journal of neurophysiology · 2017Article
- Schizophrenia-like phenotypes in mice with NMDA receptor ablation in intralaminar thalamic nucleus cells and gene therapy-based reversal in adults.Translational psychiatry · 2017Article
- Spatial and temporal boundaries of NMDA receptor hypofunction leading to schizophrenia.NPJ schizophrenia · 2017Article
- Knockout of NMDA-receptors from parvalbumin interneurons sensitizes to schizophrenia-related deficits induced by MK-801.Translational psychiatry · 2016Article
- Functional Uncoupling NMDAR NR2A Subunit from PSD-95 in the Prefrontal Cortex: Effects on Behavioral Dysfunction and Parvalbumin Loss after Early-Life Stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Pharmacological and genetic studies support a role for NMDA receptor (NMDAR) hypofunction in the etiology of schizophrenia. We have previously demonstrated that NMDAR obligatory subunit 1 (GluN1) deletion in corticolimbic interneurons during early postnatal development is sufficient to confer schizophrenia-like phenotypes in mice. However, the consequence of NMDAR hypofunction in cortical excitatory neurons is not well delineated. Here, we characterize a conditional knockout mouse strain (CtxGluN1 KO mice), in which postnatal GluN1 deletion is largely confined to the excitatory neurons in layer II/III of the medial prefrontal cortex and sensory cortices, as evidenced by the lack of GluN1 mRNA expression in in situ hybridization immunocytochemistry as well as the lack of NMDA currents with in vitro recordings. Mutants were impaired in prepulse inhibition of the auditory startle reflex as well as object-based short-term memory. However, they did not exhibit impairments in additional hallmarks of schizophrenia-like phenotypes (e.g. spatial working memory, social behavior, saccharine preference, novelty and amphetamine-induced hyperlocomotion, and anxiety-related behavior). Furthermore, upon administration of the NMDA receptor antagonist, MK-801, there were no differences in locomotor activity versus controls. The mutant mice also showed negligible levels of reactive oxygen species production following chronic social isolation, and recording of miniature-EPSC/IPSCs from layer II/III excitatory neurons in medial prefrontal cortex suggested no alteration in GABAergic activity. All together, the mutant mice displayed cognitive deficits in the absence of additional behavioral or cellular phenotypes reflecting schizophrenia pathophysiology. Thus, NMDAR hypofunction in prefrontal and cortical excitatory neurons may recapitulate only a cognitive aspect of human schizophrenia symptoms.
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