ArticleFrontiers in cellular neuroscience2015
Cocaine promotes oxidative stress and microglial-macrophage activation in rat cerebellum.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Exploring cannabidiol effects on inflammatory markers in individuals with cocaine use disorder: a randomized controlled trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Trial
- The landscape of cocaine cytotoxicity and the role of sigma-1 receptor modulation and adulterant synergism.Archives of toxicology · 2026Review
- From Neuroadaptation to Neuroprogression: Rethinking Chronic Cocaine Exposure Through a Model of Cocaine-Related Cerebropathy.Journal of clinical medicine · 2026Article
- The effects of abused drugs on ferroptosis pathways: potential therapeutic targets for substance use disorders.Frontiers in cellular neuroscience · 2026Review
- Up-regulation of Oxidative Burden, NFκB, and D1 Receptor Is Involved in the Neuropsychotoxic Behaviors Induced by Camfetamine, a New Psychoactive Substance; Involvements of the Neuromodulation by GPx-1 Gene.Neurochemical research · 2025Article
- Protective Effects of N-Acetylcysteine in Alleviating Cocaine-Mediated Microglial Activation and Neuroinflammation.Biology · 2025Article
- Distinct circulating monocyte profiles in chronic cannabis users compared to cocaine users without changes in plasma levels of proinflammatory cytokines and LPS.NeuroImmune pharmacology and therapeutics · 2025Article
- Aging and "Age-Related" Diseases - What Is the Relation?Aging and disease · 2024Review
- Substance Use and Addiction.Advances in neurobiology · 2024Review
- Role of Dysregulated Autophagy in HIV Tat, Cocaine, and cART Mediated NLRP3 Activation in Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- DNA methylation in cocaine use disorder-An epigenome-wide approach in the human prefrontal cortex.Frontiers in psychiatry · 2023Article
- The Significance of NLRP Inflammasome in Neuropsychiatric Disorders.Brain sciences · 2022Review
- Nuclear factor kappa B signaling within the rat nucleus accumbens core sex-dependently regulates cue-induced cocaine seeking and matrix metalloproteinase-9 expression.Brain, behavior, and immunity · 2022Article
- Review
- NLRP3 Inflammasome Blockade Reduces Cocaine-Induced Microglial Activation and Neuroinflammation.Molecular neurobiology · 2021Article
- Psychoactive Drugs-From Chemical Structure to Oxidative Stress Related to Dopaminergic Neurotransmission. A Review.Antioxidants (Basel, Switzerland) · 2021Review
- Chinese Herbal Medicine for the Treatment of Depression: Effects on the Neuroendocrine-Immune Network.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Importance of Redox Equilibrium in the Pathogenesis of Psoriasis-Impact of Antioxidant-Rich Diet.Nutrients · 2020Review
- MicroRNA134 of Ventral Hippocampus Is Involved in Cocaine Extinction-Induced Anxiety-like and Depression-like Behaviors in Mice.Molecular therapy. Nucleic acids · 2020Article
- Mitigation of cocaine-mediated mitochondrial damage, defective mitophagy and microglial activation by superoxide dismutase mimetics.Autophagy · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different mechanisms have been suggested for cocaine neurotoxicity, including oxidative stress alterations. Nuclear factor kappa B (NF-κB), considered a sensor of oxidative stress and inflammation, is involved in drug toxicity and addiction. NF-κB is a key mediator for immune responses that induces microglial/macrophage activation under inflammatory processes and neuronal injury/degeneration. Although cerebellum is commonly associated to motor control, muscular tone, and balance. Its relation with addiction is getting relevance, being associated to compulsive and perseverative behaviors. Some reports indicate that cerebellar microglial activation induced by cannabis or ethanol, promote cerebellar alterations and these alterations could be associated to addictive-related behaviors. After considering the effects of some drugs on cerebellum, the aim of the present work analyzes pro-inflammatory changes after cocaine exposure. Rats received daily 15 mg/kg cocaine i.p., for 18 days. Reduced and oxidized forms of glutathione (GSH) and oxidized glutathione (GSSG), glutathione peroxidase (GPx) activity and glutamate were determined in cerebellar homogenates. NF-κB activity, CD68, and GFAP expression were determined. Cerebellar GPx activity and GSH/GSSG ratio are significantly decreased after cocaine exposure. A significant increase of glutamate concentration is also observed. Interestingly, increased NF-κB activity is also accompanied by an increased expression of the lysosomal mononuclear phagocytic marker ED1 without GFAP alterations. Current trends in addiction biology are focusing on the role of cerebellum on addictive behaviors. Cocaine-induced cerebellar changes described herein fit with previosus data showing cerebellar alterations on addict subjects and support the proposed role of cerebelum in addiction.
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