ArticleACS chemical neuroscience2019
Methamphetamine Activates Toll-Like Receptor 4 to Induce Central Immune Signaling within the Ventral Tegmental Area and Contributes to Extracellular Dopamine Increase in the Nucleus Accumbens Shell.
Article in ACS chemical neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 91 citations in OpenAlex.
- The neuroimmune-glutamate hypothesis of addiction.Neuroscience and biobehavioral reviews · 2026Review
- Morphine and methamphetamine trigger divergent post-transcriptional neuroimmune landscapes in the dorsal striatum.bioRxiv : the preprint server for biology · 2026Article
- Stimulant use disorder indicative of increased serum soluble intercellular adhesion molecule-1 concentrations with altered brain reward and interoceptive processing.Brain, behavior, and immunity · 2026Observational
- Article
- Worldwide Research Trends on Substance Use Disorder-Related Inflammatory Imbalances: A Bibliometric Analysis.CNS neuroscience & therapeutics · 2025Article
- Novel neurotherapeutic targets for substance use disorders: Neuroplasticity, neuroinflammation, gasotransmitters and non-canonical organ systems.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Ibudilast-Mediated Suppression of Neuronal TLR4 in the Prefrontal Cortex Mitigates Methamphetamine-Induced Neuroinflammation and Addictive Behaviours.Addiction biology · 2025Article
- Genes, Cognition, and Their Interplay in Methamphetamine Use Disorder.Biomolecules · 2025Review
- The interaction between central and peripheral immune systems in methamphetamine use disorder: current status and future directions.Journal of neuroinflammation · 2025Review
- Single-Cell RNA-Seq Uncovers Robust Glial Cell Transcriptional Changes in Methamphetamine-Administered Mice.International journal of molecular sciences · 2025Article
- Therapeutic targeting of neuroinflammation in methamphetamine use disorder.Future medicinal chemistry · 2025Review
- Pharmacological Perspective on the Neurobiology of PI3K-Akt-mTOR Signalling in Opioid Dependence.CNS & neurological disorders drug targets · 2025Review
- The Evolution of Illicit-Drug Detection: From Conventional Approaches to Cutting-Edge Immunosensors-A Comprehensive Review.Biosensors · 2024Review
- Microglia contribute to methamphetamine reinforcement and reflect persistent transcriptional and morphological adaptations to the drug.Brain, behavior, and immunity · 2024Article
- Microglia in neuroimmunopharmacology and drug addiction.Molecular psychiatry · 2024Review
- Influence of Bariatric Surgery on Gut Microbiota Composition and Its Implication on Brain and Peripheral Targets.Nutrients · 2024Review
- Microglia contribute to methamphetamine reinforcement and reflect persistent transcriptional and morphological adaptations to the drug.bioRxiv : the preprint server for biology · 2024Article
- Substance Use and Addiction.Advances in neurobiology · 2024Review
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- The Magic Methyl and Its Tricks in Drug Discovery and Development.Pharmaceuticals (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Methamphetamine (METH) is a globally abused, highly addictive stimulant. While investigations of the rewarding and motivational effects of METH have focused on neuronal actions, increasing evidence suggests that METH can also target microglia, the innate immune cells of the central nervous system, causing release of proinflammatory mediators and therefore amplifying the reward changes in the neuronal activity induced by METH. However, how METH induces neuroinflammatory responses within the central nervous system (CNS) is unknown. Herein, we provide direct evidence that METH creates neuroinflammation, at least in part, via the activation of the innate immune Toll-like receptor 4 (TLR4). Biophysical studies revealed that METH bound to MD-2, the key coreceptor of TLR4. Molecular dynamics simulations showed METH binding stabilized the active heterotetramer (TLR4/MD-2)
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Registered trials
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.