ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
Parvalbumin cell ablation of NMDA-R1 causes increased resting network excitability with associated social and self-care deficits.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 117 citations in OpenAlex.
- A Dual Prediction Error Populations Model of Schizophrenia Spectrum Disorders: Bridging NMDA Hypofunction and Gain Hyperfunction.Schizophrenia bulletin · 2026Article
- Synaptic dysfunction and adaptation after NMDA receptor ablation in the mouse medial prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- GluK1 kainate receptors in parvalbumin interneurons modulate cortico-hippocampal network dynamics during social behavior.Translational psychiatry · 2026Article
- Protein-protein interaction-interfering peptide rescues dysregulated NMDA receptor signaling.JCI insight · 2026Article
- GluN2A-NMDA receptor inhibition disinhibits the prefrontal cortex, reduces forced swim immobility, and impairs sensorimotor gating.Acta pharmacologica Sinica · 2026Article
- Early postnatal NMDA receptor ablation in cortical interneurons impairs affective state discrimination and social functioning.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Resting-state EEG and MEG gamma frequencies in schizophrenia: a systematic review and exploratory power-spectrum metanalysis.Schizophrenia (Heidelberg, Germany) · 2025Review
- Article
- Clinical phenotype and functional influence of GRIN2A variants in epilepsy-aphasia syndrome.Epilepsia open · 2024Article
- Discovering functional interactions among schizophrenia-risk genes by combining behavioral genetics with cell biology.Neuroscience and biobehavioral reviews · 2024Review
- Brain region-specific action of ketamine as a rapid antidepressant.Science (New York, N.Y.) · 2024Article
- Serine racemase deletion alters adolescent social behavior and whole-brain cFos activation.Frontiers in psychiatry · 2024Article
- Gamma Oscillations as a Biomarker of Neural Circuit Function in Psychosis: Where Are We, and Where Do We Go from Here?Advances in neurobiology · 2024Review
- The Use of Event-Related Potentials in the Study of Schizophrenia: An Overview.Advances in neurobiology · 2024Review
- Theta-frequency medial septal nucleus deep brain stimulation increases neurovascular activity in MK-801-treated mice.Frontiers in neuroscience · 2024Article
- D-serine reconstitutes synaptic and intrinsic inhibitory control of pyramidal neurons in a neurodevelopmental mouse model for schizophrenia.Nature communications · 2023Article
- A Network Model of the Modulation of γ Oscillations by NMDA Receptors in Cerebral Cortex.eNeuro · 2023Article
- GluN2D Subunit in Parvalbumin Interneurons Regulates Prefrontal Cortex Feedforward Inhibitory Circuit and Molecular Networks Relevant to Schizophrenia.Biological psychiatry · 2023Article
- Diminished activity-dependent BDNF signaling differentially causes autism-like behavioral deficits in male and female mice.Frontiers in psychiatry · 2023Article
- Pathway-specific contribution of parvalbumin interneuron NMDARs to synaptic currents and thalamocortical feedforward inhibition.Molecular psychiatry · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
NMDA-receptor (NMDAR) hypofunction is strongly implicated in the pathophysiology of schizophrenia. Several convergent lines of evidence suggest that net excitation propagated by impaired NMDAR signaling on GABAergic interneurons may be of particular interest in mediating several aspects of schizophrenia. However, it is unclear which behavioral domains are governed by a net increase of excitation and whether modulating downstream GABAergic signaling can reverse neural and thus behavioral deficits. The current study determines the selective contributions of NMDAR dysfunction on PV-containing interneurons to electrophysiological, cognitive, and negative-symptom-related behavioral phenotypes of schizophrenia using mice with a PVcre-NR1flox-driven ablation of NR1 on PV-containing interneurons. In addition, we assessed the efficacy of one agent that directly modulates GABAergic signaling (baclofen) and one agent that indirectly modifies NMDAR-mediated signaling through antagonism of mGluR5 receptors (2-methyl-6-(phenylethynyl) pyridine (MPEP)). The data indicate that loss of NMDAR function on PV interneurons impairs self-care and sociability while increasing N1 latency and baseline gamma power, and reducing induction and maintenance of long-term potentiation. Baclofen normalized baseline gamma power without corresponding effects on behavior. MPEP further increased N1 latency and reduced social behavior in PVcre/NR1+/+ mice. These two indices were negatively correlated before and following MPEP such that as N1 latency increases, sociability decreases. This finding suggests a predictive role for N1 latency with respect to social function. Although previous data suggest that MPEP may be beneficial for core features of autism spectrum disorders, current data suggest that such effects require intact function of NMDAR on PV interneurons.
Indexed as
Identifiers
What OpenQuestion holds
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.