ArticleScientific reports2021
Delayed-matching-to-position working memory in mice relies on NMDA-receptors in prefrontal pyramidal cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed.
- GlyT1 inhibition enhances working memory in the mouse TUNL task and normalizes NMDA antagonist-induced network activity.Psychopharmacology · 2026Article
- Prefrontal parvalbumin neurons mediate working memory in a task demand-dependent manner.Nature communications · 2026Article
- Quantifying nonmnemonic strategies in two-alternative forced-choice delayed matching and nonmatching-to-position tasks in mice (Mus musculus) using automated video tracking technologies.Learning & behavior · 2026Article
- Operant House: A versatile open-source platform for automated operant conditioning testing of mice in home cages.PloS one · 2026Article
- Acute optogenetic induction of the prodromal endophenotype of CA1 hyperactivity causes schizophrenia-related deficits in cognition and salience attribution.Schizophrenia (Heidelberg, Germany) · 2024Article
- Article
- Presynaptic Rac1 in the hippocampus selectively regulates working memory.bioRxiv : the preprint server for biology · 2024Article
- The "psychiatric" neuron: the psychic neuron of the cerebral cortex, revisited.Frontiers in human neuroscience · 2024Review
- Generation of Rare Human NMDA Receptor Variants in Mice.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Spatial Learning Drives Rapid Goal Representation in Hippocampal Ripples without Place Field Accumulation or Goal-Oriented Theta Sequences.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Distinct contributions of GluA1-containing AMPA receptors of different hippocampal subfields to salience processing, memory and impulse control.Translational psychiatry · 2022Article
- Open-source, Python-based, hardware and software for controlling behavioural neuroscience experiments.eLife · 2022Article
- An integrated cytokine and kynurenine network as the basis of neuroimmune communication.Frontiers in neuroscience · 2022Review
- Decision Making in Mice During an Optimized Touchscreen Spatial Working Memory Task Sensitive to Medial Prefrontal Cortex Inactivation and NMDA Receptor Hypofunction.Frontiers in neuroscience · 2022Article
- A low-cost open-source 5-choice operant box system optimized for electrophysiology and optophysiology in mice.Scientific reports · 2021Article
- Apparatus design and behavioural testing protocol for the evaluation of spatial working memory in mice through the spontaneous alternation T-maze.Scientific reports · 2021Article
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
A hypofunction of N-methyl-D-aspartate glutamate receptors (NMDARs) has been implicated in the pathogenesis of schizophrenia by clinical and rodent studies. However, to what extent NMDAR-hypofunction in distinct cell-types across the brain causes different symptoms of this disease is largely unknown. One pharmaco-resistant core symptom of schizophrenia is impaired working memory (WM). NMDARs have been suggested to mediate sustained firing in excitatory neurons of the prefrontal cortex (PFC) that might underlie WM storage. However, if NMDAR-hypofunction in prefrontal excitatory neurons may indeed entail WM impairments is unknown. We here investigated this question in mice, in which NMDARs were genetically-ablated in PFC excitatory cells. This cell type-selective NMDAR-hypofunction caused a specific deficit in a delayed-matching-to-position (DMTP) 5-choice-based operant WM task. In contrast, T-maze rewarded alternation and several psychological functions including attention, spatial short-term habituation, novelty-processing, motivation, sociability, impulsivity, and hedonic valuation remained unimpaired at the level of GluN1-hypofunction caused by our manipulation. Our data suggest that a hypofunction of NMDARs in prefrontal excitatory neurons may indeed cause WM impairments, but are possibly not accounting for most other deficits in schizophrenia.
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