ArticlePsychopharmacology2015
Cortical GluN2B deletion attenuates punished suppression of food reward-seeking.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Punishment resistance for cocaine is associated with inflexible habits in rats.Addiction neuroscience · 2024Article
- Making and breaking habits: Revisiting the definitions and behavioral factors that influence habits in animals.Journal of the experimental analysis of behavior · 2024Review
- Neurobiological Basis of Aversion-Resistant Ethanol Seeking inMetabolites · 2022Article
- Neural correlates and determinants of approach-avoidance conflict in the prelimbic prefrontal cortex.eLife · 2021Article
- Better living through understanding the insula: Why subregions can make all the difference.Neuropharmacology · 2021Review
- Advances in understanding meso-cortico-limbic-striatal systems mediating risky reward seeking.Journal of neurochemistry · 2021Review
- Recent Perspectives on Sex Differences in Compulsion-Like and Binge Alcohol Drinking.International journal of molecular sciences · 2021Review
- Aversion-resistant fentanyl self-administration in mice.Psychopharmacology · 2021Article
- Behavioral and synaptic alterations relevant to obsessive-compulsive disorder in mice with increased EAAT3 expression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- NMDA receptor deletion on dopamine neurons disrupts visual discrimination and reversal learning.Neuroscience letters · 2019Article
- GluN2B Subunit of the NMDA Receptor: The Keystone of the Effects of Alcohol During Neurodevelopment.Neurochemical research · 2019Review
- Behavioral and neural mechanisms underlying habitual and compulsive drug seeking.Progress in neuro-psychopharmacology & biological psychiatry · 2018Review
- Chronic Ethanol During Adolescence Impacts Corticolimbic Dendritic Spines and Behavior.Alcoholism, clinical and experimental research · 2017Article
- The neural basis of reversal learning: An updated perspective.Neuroscience · 2017Review
- Chronic EtOH effects on putative measures of compulsive behavior in mice.Addiction biology · 2017Article
- Mouse strain differences in punished ethanol self-administration.Alcohol (Fayetteville, N.Y.) · 2017Article
- Reduced ethanol drinking following selective cortical interneuron deletion of the GluN2B NMDA receptors subunit.Alcohol (Fayetteville, N.Y.) · 2017Article
- Do specific NMDA receptor subunits act as gateways for addictive behaviors?Genes, brain, and behavior · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleCompulsive behavior, which is a hallmark of psychiatric disorders such as addiction and obsessive-compulsive disorder, engages corticostriatal circuits. Previous studies indicate a role for corticostriatal N-methyl-D-aspartate receptors (NMDARs) in mediating compulsive-like responding for drugs of abuse, but the specific receptor subunits controlling reward-seeking in the face of punishment remain unclear.
objectivesThe current study assessed the involvement of corticostriatal GluN2B-containing NMDARs in measures of persistent and punished food reward-seeking.
methodsMice with genetic deletion of GluN2B in one of three distinct neuronal populations, cortical principal neurons, forebrain interneurons, or striatal medium spiny neurons, were tested for (1) sustained food reward-seeking when reward was absent, (2) reward-seeking under a progressive ratio schedule of reinforcement, and (3) persistent reward-seeking after a footshock punishment.
resultsMutant mice with genetic deletion of GluN2B in cortical principal neurons demonstrated attenuated suppression of reward-seeking during punishment. These mice performed normally on other behavioral measures, including an assay for pain sensitivity. Mutants with interneuronal or striatal GluN2B deletions were normal on all behavioral assays.
conclusionsCurrent findings offer novel evidence that loss of GluN2B-containing NMDARs expressed on principal neurons in the cortex results in reduced punished food reward-seeking. These data support the involvement of GluN2B subunit in cortical circuits regulating cognitive flexibility in a variety of settings, with implications for understanding the basis of inflexible behavior in neuropsychiatric disorders including obsessive-compulsive disorders (OCD) and addictions.
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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.