ArticleNeuroreport2015
Impaired discrimination learning in interneuronal NMDAR-GluN2B mutant mice.
Article in Neuroreport, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Integrating optical neuroscience tools into touchscreen operant systems.Nature protocols · 2025Review
- CXCR2 immunomodulatory therapy protects against microstructural white matter injury and gait abnormalities but does not mitigate deficits of cognition in a preclinical model of cerebral palsy.Journal of neurochemistry · 2025Article
- Article
- Neonatal administration of erythropoietin attenuates cognitive deficits in adult rats following placental insufficiency.Journal of neuroscience research · 2022Article
- Touchscreen cognitive deficits, hyperexcitability and hyperactivity in males and females using two models of Cdkl5 deficiency.Human molecular genetics · 2022Article
- Impaired cognitive flexibility following NMDAR-GluN2B deletion is associated with altered orbitofrontal-striatal function.Neuroscience · 2021Article
- Reduced exploratory behavior in neuronal nucleoredoxin knockout mice.Redox biology · 2021Article
- Prevention of age-associated neuronal hyperexcitability with improved learning and attention upon knockout or antagonism of LPAR2.Cellular and molecular life sciences : CMLS · 2021Article
- Learning and reaction times in mouse touchscreen tests are differentially impacted by mutations in genes encoding postsynaptic interacting proteins SYNGAP1, NLGN3, DLGAP1, DLGAP2 and SHANK2.Genes, brain, and behavior · 2021Article
- Impaired cognitive flexibility following NMDAR-GluN2B deletion is associated with altered orbitofrontal-striatal function.Neuroscience · 2019Article
- Cortico-hippocampal GluN2B is essential for efficient visual-spatial discrimination learning in a touchscreen paradigm.Neurobiology of learning and memory · 2018Article
- Behavioral and neuroanatomical approaches in models of neurodevelopmental disorders: opportunities for translation.Current opinion in neurology · 2018Review
- Reduced ethanol drinking following selective cortical interneuron deletion of the GluN2B NMDA receptors subunit.Alcohol (Fayetteville, N.Y.) · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Previous studies have established a role for N-methyl-D-aspartate receptor (NMDAR) containing the GluN2B subunit in efficient learning behavior on a variety of tasks. Recent findings have suggested that NMDAR on GABAergic interneurons may underlie the modulation of striatal function necessary to balance efficient action with cortical excitatory input. Here we investigated how loss of GluN2B-containing NMDAR on GABAergic interneurons altered corticostriatal-mediated associative learning. Mutant mice (floxed-GluN2B×Ppp1r2-Cre) were generated to produce loss of GluN2B on forebrain interneurons and phenotyped on a touchscreen-based pairwise visual learning paradigm. We found that the mutants showed normal performance during Pavlovian and instrumental pretraining, but were significantly impaired on a discrimination learning task. Detailed analysis of the microstructure of discrimination performance revealed reduced win→stay behavior in the mutants. These results further support the role of NMDAR, and GluN2B in particular, on modulation of striatal function necessary for efficient choice behavior and suggest that NMDAR on interneurons may play a critical role in associative learning.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.