A neurotoxic regimen of methamphetamine exacerbates the febrile and neuroinflammatory response to a subsequent peripheral immune stimulus
Open accessAbstract
Methamphetamine (MA) use is associated with activation of microglia and, at high doses, can induce neurotoxicity. Given the changes in the neuroinflammatory environment associated with MA, we investigated whether MA administration would interfere with the thermoregulatory and neuroinflammatory response to a subsequent peripheral immune stimulus. C57BL6/J mice were given four i.p. injections of either 5 mg/kg MA or saline at two hour intervals. Twenty-four hours following the first MA injection, mice were given 100 μg/kg LPS or saline i.p. and blood and brains were collected. Here we report that mice exposed to MA developed higher fevers in response to LPS than did those given LPS alone. MA also exacerbated the LPS-induced increase in central cytokine mRNA. MA alone increased microglial Iba1 expression and expression was further increased when mice were exposed to both MA and LPS, suggesting that MA not only activated microglia but also influenced their response to a peripheral immune stimulus. Taken together, these data show that MA administration exacerbates the normal central immune response, most likely by altering microglia.
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Prior methamphetamine administration potentiates microglial activation induced by LPS.
“prior Meth also potentiated the microglial activation induced by LPS (Buchanan et al., 2010)”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Buchanan et al., 2010
Prior methamphetamine administration potentiates the pro-inflammatory cytokine response to LPS across several brain regions including striatum, hypothalamus, hippocampus, cortex, and cerebellum.
“prior Meth administration potentiated the pro-inflammatory cytokine response to LPS across several brain regions including striatum, hypothalamus, hippocampus, cortex, and cerebellum”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Buchanan et al., 2010
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- Authors
- Buchanan, J. B., Sparkman, N. L., & Johnson, R. W.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- Corresponding author
- Buchanan, Jessica B
- ORCID
- Johnson, Rodney W
- Venue
- Journal of Neuroinflammation
- Published
- 2010
- Volume
- 7
- Issue
- 1
- Pages
- 82
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC2995792
- OpenAlex
- W2154092635
- Cited by
- 35
- References
- 41
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 1 · 2019: 2 · 2018: 9 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 1
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Drug Abuse (R21DA024443, DA024443)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Thermal Regulation in Medicine
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- methamphetamine, neuroinflammation, microglial activation, fever, lipopolysaccharide, cytokine expression, thermoregulation, neurotoxicity, Iba1, brain immune response, C57BL/6J mice
- MeSH terms
- Animals, Body Temperature, Calcium-Binding Proteins, Fever, Lipopolysaccharides, Male, Methamphetamine, Mice, Inbred C57BL, Microfilament Proteins, Motor Activity, RNA, Messenger, Cytokines, Microglia, Mice
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