ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2021
Astrocyte-derived TNF and glutamate critically modulate microglia activation by methamphetamine.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The trial behind it
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Who cites it
49 citing papers in PubMed, 80 citations in OpenAlex.
- Effects of chronic methamphetamine exposure on rewarding behavior and neurodegeneration markers in adult mice.Psychopharmacology · 2023Trial
- The actions of morphine on microglia and the underlying effects on associated adverse effects.Psychopharmacology · 2026Review
- Molecular Mechanisms of Hippocampal Synaptic Plasticity Disruption Induced by Chronic Methamphetamine Exposure: A Narrative Review.Cellular and molecular neurobiology · 2026Review
- Multimodal MRI Reveals Brain Structural Differences and Executive Dysfunction in Early Methamphetamine Abstinence.Brain and behavior · 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
- Astrocytic Netrin-1 modulates stress-induced anxiety susceptibility in mice through ADAM17-mediated TNFα shedding.Journal of neuroinflammation · 2026Article
- The effect of neuroimmune signalling on drug addiction.Frontiers in pharmacology · 2026Review
- Mechanisms and therapeutic advances of gut metabolites in the regulation of neuroimmune inflammatory diseases.Frontiers in immunology · 2026Review
- The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise.Journal of neuroimmunology · 2025Review
- Article
- Profilin 1 controls a microglial cytoskeleton checkpoint to prevent senescence and premature synaptic decline.Journal of neuroinflammation · 2025Article
- Intersectin1/cdc42 signaling regulates methamphetamine-induced neuronal remodeling in the hippocampus.Cellular and molecular life sciences : CMLS · 2025Article
- Beyond the gut: decoding the gut-immune-brain axis in health and disease.Cellular & molecular immunology · 2025Review
- The interaction between central and peripheral immune systems in methamphetamine use disorder: current status and future directions.Journal of neuroinflammation · 2025Review
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- A ketogenic diet regulates microglial activation to treat drug addiction.Frontiers in pharmacology · 2025Review
- Cardiomyocyte-derived exosomes carrying miR-181a-5p facilitate heart-brain crosstalk and exacerbate methamphetamine dependence in rats.Frontiers in pharmacology · 2025Article
- Novel human iPSC models of neuroinflammation in neurodegenerative disease and regenerative medicine.Trends in immunology · 2024Review
- Nimodipine attenuates neuroinflammation and delayed apoptotic neuronal death induced by trimethyltin in the dentate gyrus of mice.Journal of molecular histology · 2024Article
- Inflammaging and Brain Aging.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Methamphetamine (Meth) is a powerful illicit psychostimulant, widely used for recreational purposes. Besides disrupting the monoaminergic system and promoting oxidative brain damage, Meth also causes neuroinflammation, contributing to synaptic dysfunction and behavioral deficits. Aberrant activation of microglia, the largest myeloid cell population in the brain, is a common feature in neurological disorders triggered by neuroinflammation. In this study, we investigated the mechanisms underlying the aberrant activation of microglia elicited by Meth in the adult mouse brain. We found that binge Meth exposure caused microgliosis and disrupted risk assessment behavior (a feature that usually occurs in individuals who abuse Meth), both of which required astrocyte-to-microglia crosstalk. Mechanistically, Meth triggered a detrimental increase of glutamate exocytosis from astrocytes (in a process dependent on TNF production and calcium mobilization), promoting microglial expansion and reactivity. Ablating TNF production, or suppressing astrocytic calcium mobilization, prevented Meth-elicited microglia reactivity and re-established risk assessment behavior as tested by elevated plus maze (EPM). Overall, our data indicate that glial crosstalk is critical to relay alterations caused by acute Meth exposure.
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What OpenQuestion holds
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.