Methamphetamine-induced neuroinflammation and neuronal dysfunction in the mice hippocampus: preventive effect of indomethacin
Abstract
Methamphetamine (METH) causes irreversible damage to brain cells leading to neurological and psychiatric abnormalities. However, the mechanisms underlying life-threatening effects of acute METH intoxication remain unclear. Indeed, most of the hypotheses focused on intra-neuronal events, such as dopamine oxidation, oxidative stress and excitotoxicity. Yet, recent reports suggested that glia may contribute to METH-induced neuropathology. In the present study, we investigated the hippocampal dysfunction induced by an acute high dose of METH (30 mg/kg; intraperitoneal injection), focusing on the inflammatory process and changes in several neuronal structural proteins. For that, 3-month-old male wild-type C57BL/6J mice were killed at different time-points post-METH. We observed that METH caused an inflammatory response characterized by astrocytic and microglia reactivity, and tumor necrosis factor (TNF) system alterations. Indeed, glial fibrillary acidic protein (GFAP) and CD11b immunoreactivity were upregulated, likewise TNF-alpha and TNF receptor 1 protein levels. Furthermore, the effect of METH on hippocampal neurons was also investigated, and we observed a downregulation in beta III tubulin expression. To clarify the possible neuronal dysfunction induced by METH, several neuronal proteins were analysed. Syntaxin-1, calbindin D28k and tau protein levels were downregulated, whereas synaptophysin was upregulated. We also evaluated whether an anti-inflammatory drug could prevent or diminish METH-induced neuroinflammation, and we concluded that indomethacin (10 mg/kg; i.p.) prevented METH-induced glia activation and both TNF system and beta III tubulin alterations. In conclusion, we demonstrated that METH triggers an inflammatory process and leads to neuronal dysfunction in the hippocampus, which can be prevented by an anti-inflammatory treatment.
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Indomethacin pretreatment can prevent the neuroinflammatory effects of methamphetamine.
“indomethacin (a non-steroidal anti-inflammatory) pretreatment can prevent the neuroinflammatory effects of Meth (Goncalves 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 Goncalves et al., 2010
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“…number of reports show that Meth activates microglia (Bowyer and Ali, 2006; Buchanan et al., 2010; Escubedo et al., 1998; Fantegrossi et al., 2008; Goncalves et al., 2010; Guilarte et al., 2003; Ladenheim et al., 2000; LaVoie et al., 2004; Pubill et al., 2003; Sekine et al., 2008; Sharma and…”
BackgroundBuchanan, J. B., Sparkman, N. L., & Johnson, R. W. (2010) · Journal of Neuroinflammation · doi:10.1186/1742-2094-7-82 · Cited by 35 · see citing works
- Authors
- Gonçalves, J., Baptista, S., Martins, T., Milhazes, N., Borges, F., Ribeiro, C. F., Malva, J. O., & Silva, A. P.
- Affiliations
- University of Coimbra (PT)
- Centro de Neurociências e Biologia Celular (PT)
- Universidade do Porto (PT)
- ORCID
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2010-01
- Volume
- 31
- Issue
- 2
- Pages
- 315-326
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2163407153
- Cited by
- 152
- References
- 76
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 8 · 2023: 11 · 2022: 10 · 2021: 12 · 2020: 12 · 2019: 11 · 2018: 12 · 2017: 9 · 2016: 3 · 2015: 10 · 2014: 11 · 2013: 6 · 2012: 15
- FWCI
- 5.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- methamphetamine, neuroinflammation, hippocampus, indomethacin, glial activation, astrocytes, microglia, TNF-α, TNF receptor 1, glial fibrillary acidic protein, CD11b, TUBB3, neuronal dysfunction, anti-inflammatory therapy, synaptophysin, tau protein, calbindin-D28k, syntaxin-1
- MeSH terms
- Disks Large Homolog 4 Protein, Central Nervous System Stimulants, Animals, Anti-Inflammatory Agents, Non-Steroidal, Glial Fibrillary Acidic Protein, Hippocampus, Indomethacin, Inflammation, Male, Membrane Proteins, Methamphetamine, Mice, Inbred C57BL, Neuroglia, Neurons, Tumor Necrosis Factor-alpha, Synaptophysin, CD11b Antigen, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Intracellular Signaling Peptides and Proteins, Qa-SNARE Proteins, Synaptosomal-Associated Protein 25, Mice, Guanylate Kinases
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