ArticleFrontiers in behavioral neuroscience2015
Targeting Glia with N-Acetylcysteine Modulates Brain Glutamate and Behaviors Relevant to Neurodevelopmental Disorders in C57BL/6J Mice.
Article in Frontiers in behavioral neuroscience, 2015. 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, 36 citations in OpenAlex.
- The Central Nervous System Modulatory Activities of N-Acetylcysteine: A Synthesis of Two Decades of Evidence.Current issues in molecular biology · 2025Review
- Article
- Intestine and brain TLR-4 modulation following N-acetyl-cysteine treatment in NEC rodent model.Scientific reports · 2023Article
- Effect of N-Acetylcysteine on Sleep: Impacts of Sex and Time of Day.Antioxidants (Basel, Switzerland) · 2023Article
- Neuroimmune transcriptome changes in patient brains of psychiatric and neurological disorders.Molecular psychiatry · 2023Article
- Chronic dietary supplementation with nicotinamide riboside reduces sleep need in the laboratory mouse.Sleep advances : a journal of the Sleep Research Society · 2023Article
- The Potential of N-Acetyl-L-Cysteine (NAC) in the Treatment of Psychiatric Disorders.CNS drugs · 2022Review
- N-Acetylcysteine Mitigates Social Dysfunction in a Rat Model of Autism Normalizing Glutathione Imbalance and the Altered Expression of Genes Related to Synaptic Function in Specific Brain Areas.Frontiers in psychiatry · 2022Article
- Positron Emission Tomography in the Neuroimaging of Autism Spectrum Disorder: A Review.Frontiers in neuroscience · 2022Review
- Chronic N-acetylcysteine treatment improves anhedonia and cognition in a mouse model of the schizophrenia prodrome.Frontiers in behavioral neuroscience · 2022Article
- Increasing Nrf2 Activity as a Treatment Approach in Neuropsychiatry.Molecular neurobiology · 2021Review
- The potential ofPsychopharmacology · 2021Review
- Fetal Neuroprotective Strategies: Therapeutic Agents and Their Underlying Synaptic Pathways.Frontiers in synaptic neuroscience · 2021Review
- Sex differences and Tat expression affect dopaminergic receptor expression and response to antioxidant treatment in methamphetamine-sensitized HIV Tat transgenic mice.Neuropharmacology · 2020Article
- Drug-responsive autism phenotypes in the 16p11.2 deletion mouse model: a central role for gene-environment interactions.Scientific reports · 2020Article
- Histomorphological evaluations on the frontal cortex extrapyramidal cell layer following administration of N-Acetyl cysteine in aluminum induced neurodegeneration rat model.Metabolic brain disease · 2020Article
- Antioxidants Reduce Muscular Dystrophy in theAntioxidants (Basel, Switzerland) · 2020Article
- Hippocampal Hyperactivity as a Druggable Circuit-Level Origin of Aberrant Salience in Schizophrenia.Frontiers in pharmacology · 2020Review
- Glial Contribution to Excitatory and Inhibitory Synapse Loss in Neurodegeneration.Frontiers in cellular neuroscience · 2019Review
- Effects of N-acetylcysteine on brain glutamate levels and resting perfusion in schizophrenia.Psychopharmacology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An imbalance between excitatory (E) glutamate and inhibitory (I) GABA transmission may underlie neurodevelopmental conditions such as autism spectrum disorder (ASD) and schizophrenia. This may be direct, through alterations in synaptic genes, but there is increasing evidence for the importance of indirect modulation of E/I balance through glial mechanisms. Here, we used C57BL/6J mice to test the hypothesis that striatal glutamate levels can be shifted by N-acetylcysteine (NAC), which acts at the cystine-glutamate antiporter of glial cells. Striatal glutamate was quantified in vivo using proton magnetic resonance spectroscopy. The effect of NAC on behaviors relevant to ASD was examined in a separate cohort. NAC induced a time-dependent decrease in striatal glutamate, which recapitulated findings of lower striatal glutamate reported in ASD. NAC-treated animals were significantly less active and more anxious in the open field test; and NAC-treated females had significantly impaired prepulse inhibition of startle response. This at least partly mimics greater anxiety and impaired sensorimotor gating reported in neurodevelopmental disorders. Thus glial mechanisms regulate glutamate acutely and have functional consequences even in adulthood. Glial cells may be a potential drug target for the development of new therapies for neurodevelopmental disorders across the life-span.
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Registered trials
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