ArticleJournal of neural transmission (Vienna, Austria : 1996)2009
Lipopolysaccharide mitagates methamphetamine-induced striatal dopamine depletion via modulating local TNF-alpha and dopamine transporter expression.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Changes in Artemin Correlate with Anxiety- and Depression-like Behaviors in a Lipopolysaccharide-Induced Rat Neuroinflammation Model.Biomolecules · 2025Article
- Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023Review
- Gut microbiota dysbiosis: The potential mechanisms by which alcohol disrupts gut and brain functions.Frontiers in microbiology · 2022Review
- Aiding and Abetting Anhedonia: Impact of Inflammation on the Brain and Pharmacological Implications.Pharmacological reviews · 2021Review
- Psychostimulant Use Disorder, an Unmet Therapeutic Goal: Can Modafinil Narrow the Gap?Frontiers in neuroscience · 2021Review
- Mitigating Effects ofBrain sciences · 2020Article
- Substance Use Disorder in the COVID-19 Pandemic: A Systematic Review of Vulnerabilities and Complications.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Combination of acute intravenous methamphetamine injection and LPS challenge facilitate leukocyte infiltration into the central nervous system of C57BL/6 mice.International immunopharmacology · 2019Article
- Assessment of Striatal Dopamine Transporter Binding in Individuals With Major Depressive Disorder: In Vivo Positron Emission Tomography and Postmortem Evidence.JAMA psychiatry · 2019Article
- Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters.Pharmacological reviews · 2016Review
- The danger-associated molecular pattern HMGB1 mediates the neuroinflammatory effects of methamphetamine.Brain, behavior, and immunity · 2016Article
- Sigma receptor antagonists attenuate acute methamphetamine-induced hyperthermia by a mechanism independent of IL-1β mRNA expression in the hypothalamus.European journal of pharmacology · 2012Article
- The effects of psychostimulant drugs on blood brain barrier function and neuroinflammation.Frontiers in pharmacology · 2012Article
- Stress- and glucocorticoid-induced priming of neuroinflammatory responses: potential mechanisms of stress-induced vulnerability to drugs of abuse.Brain, behavior, and immunity · 2011Review
- A neurotoxic regimen of methamphetamine exacerbates the febrile and neuroinflammatory response to a subsequent peripheral immune stimulus.Journal of neuroinflammation · 2010Article
- A study on the mechanisms by which minocycline protects against MDMA ('ecstasy')-induced neurotoxicity of 5-HT cortical neurons.Neurotoxicity research · 2010Article
- Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity.Temperature (Austin, Tex.)Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lipopolysaccharide (LPS) treatment may affect methamphetamine (MA)-induced nigrostriatal dopamine (DA) depletion. This study was undertaken to determine the critical time window for the protective effects of LPS treatment and the underlying mechanisms. An LPS injection (1 mg/kg) 72 h before or 2 h after MA treatment [three consecutive, subcutaneous injections of MA (10 mg/kg each) at 2-h intervals] diminished the MA-induced DA depletion in mouse striatum. Such an LPS-associated effect was independent of MA-produced hyperthermia. TNF-alpha, IL-1beta, IL-6 expressions were all elevated in striatal tissues following a systemic injection with LPS, indicating that peripheral LPS treatment affected striatal pro-inflammatory cytokine expression. Striatal TNF-alpha expression was dramatically increased at 72 and 96 h after the MA treatment, while such TNF-alpha elevation was abolished by the LPS pretreatment protocol. Moreover, MA-produced activation of nuclear NFkappaB, a transcription factor following TNF-alpha activation, in striatum was abolished by the LPS (1 mg/kg) pretreatment. Furthermore, thalidomide, a TNF-alpha antagonist, treatment abolished the LPS pretreatment-associated protective effects. Pretreatment with mouse recombinant TNF-alpha in striatum diminished the MA-produced DA depletion. Finally, single LPS treatment caused a rapid down-regulation of dopamine transporter (DAT) in striatum. Taken together, we conclude that peripheral LPS treatment protects nigrostriatal DA neurons against MA-induced toxicity, in part, by reversing elevated TNF-alpha expression and subsequent signaling cascade and causing a rapid DAT down-regulation in striatum.
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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.