ArticlePloS one2014
Mice lacking NMDA receptors in parvalbumin neurons display normal depression-related behavior and response to antidepressant action of NMDAR antagonists.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 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
35 citing papers in PubMed, 70 citations in OpenAlex.
- Molecular and neural circuit mechanisms of parvalbumin (PV) neurons in depression: Insights and advances.iScience · 2026Review
- Behavioral impact of adolescent social isolation stress: A multidimensional assessment in male NMRI mice.Learning & behavior · 2026Article
- ThePhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- An automated platform for Assessing Working Memory and prefrontal circuit function.Neurobiology of stress · 2023Article
- The role of ketamine in major depressive disorders: Effects on parvalbumin-positive interneurons in hippocampus.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Mechanisms of ketamine and its metabolites as antidepressants.Biochemical pharmacology · 2022Review
- Reproducing the dopamine pathophysiology of schizophrenia and approaches to ameliorate it: a translational imaging study with ketamine.Molecular psychiatry · 2021Article
- Interneuron NMDA Receptor Ablation Induces Hippocampus-Prefrontal Cortex Functional Hypoconnectivity after Adolescence in a Mouse Model of Schizophrenia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Ketamine: The final frontier or another depressing end?Behavioural brain research · 2020Review
- GABA interneurons are the cellular trigger for ketamine's rapid antidepressant actions.The Journal of clinical investigation · 2020Article
- Rodent ketamine depression-related research: Finding patterns in a literature of variability.Behavioural brain research · 2019Review
- Neurobiology of rapid-acting antidepressants: convergent effects on GluA1-synaptic function.Molecular psychiatry · 2019Review
- NMDA 2A receptors in parvalbumin cells mediate sex-specific rapid ketamine response on cortical activity.Molecular psychiatry · 2019Article
- Molecular Pharmacology and Neurobiology of Rapid-Acting Antidepressants.Annual review of pharmacology and toxicology · 2019Review
- Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?Frontiers in psychiatry · 2019Review
- Article
- Ketamine and selective activation of parvalbumin interneurons inhibit stress-induced dendritic spine elimination.Translational psychiatry · 2018Article
- Mechanisms of ketamine action as an antidepressant.Molecular psychiatry · 2018Review
- Disinhibition of CA1 pyramidal cells by low-dose ketamine and other antagonists with rapid antidepressant efficacy.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Engaging homeostatic plasticity to treat depression.Molecular psychiatry · 2018Review
Corrections and comments
- Erratum issuedDorocic, Iskra Pollak [corrected to Pollak Dorocic, Iskra]
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The underlying circuit imbalance in major depression remains unknown and current therapies remain inadequate for a large group of patients. Discovery of the rapid antidepressant effects of ketamine--an NMDA receptor (NMDAR) antagonist--has linked the glutamatergic system to depression. Interestingly, dysfunction in the inhibitory GABAergic system has also been proposed to underlie depression and deficits linked to GABAergic neurons have been found with human imaging and in post-mortem material from depressed patients. Parvalbumin-expressing (PV) GABAergic interneurons regulate local circuit function through perisomatic inhibition and their activity is NMDAR-dependent, providing a possible link between NMDAR and the inhibitory system in the antidepressant effect of ketamine. We have therefore investigated the role of the NMDAR-dependent activity of PV interneurons for the development of depression-like behavior as well as for the response to rapid antidepressant effects of NMDAR antagonists. We used mutant mice lacking NMDA neurotransmission specifically in PV neurons (PV-Cre+/NR1f/f) and analyzed depression-like behavior and anhedonia. To study the acute and sustained effects of a single NMDAR antagonist administration, we established a behavioral paradigm of repeated exposure to forced swimming test (FST). We did not observe altered behavioral responses in the repeated FST or in a sucrose preference test in mutant mice. In addition, the behavioral response to administration of NMDAR antagonists was not significantly altered in mutant PV-Cre+/NR1f/f mice. Our results show that NMDA-dependent neurotransmission in PV neurons is not necessary to regulate depression-like behaviors, and in addition that NMDARs on PV neurons are not a direct target for the NMDAR-induced antidepressant effects of ketamine and MK801.
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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.