ArticlePsychopharmacology2018
Chronic N-acetylcysteine treatment alleviates acute lipopolysaccharide-induced working memory deficit through upregulating caveolin-1 and synaptophysin in mice.
Article in Psychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Microglial Activation Plays a Critical Role in LPS-Induced Contextual Fear Memory Consolidation Impairment and Blood-Brain Barrier Disruption.Brain and behavior · 2026Article
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- Aging-Induced Episodic-Like Memory Impairment Could be Alleviated by Melatonin Treatment via Preserving Blood-Brain Barrier Integrity and Upregulating CRTC1.CNS neuroscience & therapeutics · 2025Article
- The Effect of Disulfiram and N-Acetylcysteine, Potential Compensators for Sulfur Disorders, on Lipopolysaccharide-Induced Neuroinflammation Leading to Memory Impairment and the Metabolism of L-Cysteine Disturbance.Molecules (Basel, Switzerland) · 2025Article
- Ginsenoside Rk1 alleviates lipopolysaccharide (LPS)-induced cognitive impairment by modulating synaptic plasticity.Frontiers in pharmacology · 2025Article
- Annexin A6 mitigates neurological deficit in ischemia/reperfusion injury by promoting synaptic plasticity.CNS neuroscience & therapeutics · 2024Article
- Nicotine pretreatment alleviates MK-801-induced behavioral and cognitive deficits in mice by regulating Pdlim5/CRTC1 in the PFC.Acta pharmacologica Sinica · 2023Article
- Effect of transcranial near-infrared photobiomodulation on cognitive outcomes in D-galactose/AlClLasers in medical science · 2022Article
- Acute Nicotine Treatment Alleviates LPS-Induced Impairment of Fear Memory Reconsolidation Through AMPK Activation and CRTC1 Upregulation in Hippocampus.The international journal of neuropsychopharmacology · 2020Article
- Differential Effect of Repeated Lipopolysaccharide Treatment and Aging on Hippocampal Function and Biomarkers of Hippocampal Senescence.Molecular neurobiology · 2020Article
- D1 receptor-mediated endogenous tPA upregulation contributes to blood-brain barrier injury after acute ischaemic stroke.Journal of cellular and molecular medicine · 2020Article
- Adolescent ΔFrontiers in psychiatry · 2020Article
- Inhibition of Reactive Astrocytes with Fluorocitrate Ameliorates Learning and Memory Impairment Through Upregulating CRTC1 and Synaptophysin in Ischemic Stroke Rats.Cellular and molecular neurobiology · 2019Article
- Effect of Systemic Inflammation on Rat Attentional Function and Neuroinflammation: Possible Protective Role for Food Restriction.Frontiers in aging neuroscience · 2019Article
- Chronic Stress Weakens Connectivity in the Prefrontal Cortex: Architectural and Molecular Changes.Chronic stress (Thousand Oaks, Calif.)Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleWorking memory (WM) is a dynamic encoding process and an active representation of information over a short time. The ability to guide forthcoming behavior would be disrupted if WM was impaired by various factors including inflammation, stress, free radicals, and disease states such as schizophrenia. However, the mechanism underlying acute working memory impairment remains to be defined.
objectivesIn this study, we tested the hypothesis that decreased caveolin-1 (Cav-1) and synaptophysin (SYP) accounted for the WM impairment challenged with acute intraperitoneally lipopolysaccharide (LPS), which mimicked neuroinflammation. Delayed alternation T-maze task (DAT) was used to assess working memory of adult male C57BL/6 mice, and western blot and immunostaining were used to detect protein expression and distribution in medial prefrontal cortex (mPFC) and hippocampus.
resultsOur results showed that LPS dose-dependently induced working memory deficit accompanied by the decrease of Cav-1 and SYP in mPFC but not hippocampus. In addition, LPS significantly decreased protein level of Cav-1 and SYP in neurons by activating microglia cells. More important, 2-week N-acetylcysteine (NAC) treatment dose-dependently inhibited LPS-induced working memory deficit by improving the ability to use Lose-shift but not Win-shift strategy and significantly inhibited LPS-induced downregulation of Cav-1 and SYP in mPFC.
conclusionsTaken together, our findings demonstrate that chronic NAC treatment alleviates acute LPS-induced working memory deficit through upregulating Cav-1 and SYP in mice.
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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.