Human immunodeficiency virus-1 protein tat and methamphetamine interactions
Abstract
The human immunodeficiency virus-1 (HIV-1) affects the central nervous system (CNS) in approximately 30% of infected individuals and basal ganglia structures seem to be most affected. The HIV-1-transactivating protein, Tat, has been suggested to be pathogenically relevant in HIV-1-induced neuronal injury. The abuse of methamphetamine (METH), which is great among this patient population, also affects the basal ganglia, causing degeneration of dopaminergic terminals. In previous studies, we demonstrated that coexposure to these two toxins caused a synergistic loss of striatal dopamine and binding to the dopamine transporter (DAT), suggesting a loss of dopamine terminals. Because the loss of dopamine and DAT, however, do not necessarily reflect dopamine terminal degeneration, we have used silver staining and TH immunohistochemistry to further examine this issue. We have also examined the glial reaction using GFAP as a marker of astrocyte activation and OX-42 as a marker of activated microglia. Lastly, we have begun to explore the mechanism of synergy by investigating the role that the cytokine TNF-alpha might play in Tat + METH synergy. Our data indicate that the synergistic loss of dopamine is likely the result of dopamine terminal degeneration. This injury is not a direct result of the number of activated glia but does involve TNF-alpha.
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Acute methamphetamine potentiates chemokine expression to the HIV Tat protein.
“as well as the chemokine expression to the HIV Tat protein (Theodore et al., 2006)”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Theodore et al., 2006
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- Authors
- THEODORE, S., STOLBERG, S., CASS, W. A., & MARAGOS, W. F.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- MARAGOS, WILLIAM F.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2006-08
- Volume
- 1074
- Issue
- 1
- Pages
- 178-190
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2006097435
- Cited by
- 27
- References
- 28
- Citations by year
- 2021: 1 · 2017: 2 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 3
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG017963, AG17963)
- National Institute on Drug Abuse (DA13144, R01DA013144)
- Topics
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- HIV-1 Tat protein, methamphetamine, drug synergy, striatum, basal ganglia, dopamine transporter, astrocyte activation, microglial activation, TNF-α, neurotoxicity, HIV-associated neurocognitive disorders
- MeSH terms
- Animals, Corpus Striatum, Dopamine, Drug Synergism, Humans, Immunohistochemistry, Male, Methamphetamine, Mice, Inbred C57BL, Neuroglia, Tumor Necrosis Factor-alpha, Gene Products, tat, Silver Staining, Mice, Knockout, Mice, Rats
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