ArticleBehavioural brain research2019
Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression.
Article in Behavioural brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
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- Evaluation of the therapeutic efficacy of the dextromethorphan-bupropion combination and its mediating pathways in a mouse model of major depressive disorder.Frontiers in pharmacology · 2026Article
- Neuroinflammatory history results in overlapping transcriptional signatures with heroin exposure in the nucleus accumbens and alters responsiveness to heroin in male rats.Translational psychiatry · 2024Article
- GluN2A: A Promising Target for Developing Novel Antidepressants.The international journal of neuropsychopharmacology · 2024Review
- Immune and neural response to acute social stress in adolescent humans and rodents.Translational psychiatry · 2024Article
- First trimester human umbilical cord perivascular cells (HUCPVC) modulate the kynurenine pathway and glutamate neurotransmission in an LPS-induced mouse model of neuroinflammation.Journal of inflammation (London, England) · 2023Article
- Dysfunction of Glutamatergic Synaptic Transmission in Depression: Focus on AMPA Receptor Trafficking.Biological psychiatry global open science · 2023Review
- Intermittent systemic exposure to lipopolysaccharide-induced inflammation disrupts hippocampal long-term potentiation and impairs cognition in aging male mice.Brain, behavior, and immunity · 2023Article
- Chemogenetic activation of the HPC-mPFC pathway improves cognitive dysfunction in lipopolysaccharide -induced brain injury.Theranostics · 2023Article
- Targeting NMDA Receptors in Emotional Disorders: Their Role in Neuroprotection.Brain sciences · 2022Review
- Interactions Among Brain-Derived Neurotrophic Factor and Neuroimmune Pathways Are Key Components of the Major Psychiatric Disorders.Molecular neurobiology · 2022Review
- Acute Sleep Deprivation-Induced Anxiety and Disruption of Hypothalamic Cell Survival and Plasticity: A Mechanistic Study of Protection by Butanol Extract of Tinospora cordifolia.Neurochemical research · 2022Article
- Testing the Role of Glutamate NMDA Receptors in Peripheral Trigeminal Nociception Implicated in Migraine Pain.International journal of molecular sciences · 2022Article
- GluN2A-ERK-mTOR pathway confers a vulnerability to LPS-induced depressive-like behaviour.Behavioural brain research · 2022Article
- Anti-Inflammatory Activity ofInternational journal of molecular sciences · 2021Article
- Glycogen Synthase Kinase-3: A Focal Point for Advancing Pathogenic Inflammation in Depression.Cells · 2021Review
- Post-inflammatory behavioural despair in male mice is associated with reduced cortical glutamate-glutamine ratios, and circulating lipid and energy metabolites.Scientific reports · 2020Article
- Peripheral ProBDNF Delivered by an AAV Vector to the Muscle Triggers Depression-Like Behaviours in Mice.Neurotoxicity research · 2020Article
- Sobriety and Satiety: Is NAD+ the Answer?Antioxidants (Basel, Switzerland) · 2020Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent reports have demonstrated that lipopolysaccharide (LPS)-induced depressive-like behaviour is mediated via NMDA receptor. In this study, we further investigated the role of GluN2 A subunit of NMDA receptor in synaptic processes in the prefrontal cortex (PFC) and hippocampus of GluN2 A knockout (KO) mice in LPS-induced depressive-like behavior. Our data suggest that LPS-treated mice, lacking GluN2 A subunit, did not exhibit depressive-like behaviour. This was accompanied by unaltered levels of IL-6 and significant changes in neuroplasticity markers and glutamate receptor subunits composition in PFC and hippocampus. In particular, an immune challenge in GluN2 A KO mice resulted in unchanged PSA-NCAM levels and proBDNF increase in both brain structures as well as in increase in BDNF levels in hippocampus. Furthermore, the absence of GluN2 A resulted in increased levels of all NCAM isoforms in PFC upon LPS which was followed with a decrease in GluN1 and GluN2B subunits. The levels of AMPA receptor subunits (GluA1, GluA3, and GluA4) in the hippocampus of GluN2 A mice were unaltered upon the treatment and abundantly present in the PFC of KO mice. These results indicate that the GluN2 A subunit is critical in neuroinflammation-related depression, that its absence abolishes LPS-induced depressive phenotype, sustains PSA-NCAM levels, increases proBDNF signalling in the PFC and hippocampus and potentiates synaptic stabilization through NCAM in the PFC upon an immune challenge.
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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.