Inhibition of tumor necrosis factor-alpha signaling prevents human immunodeficiency virus-1 protein Tat and methamphetamine interaction

Shaji Theodore; Wayne A. Cass; Avindra Nath; Joseph Steiner; Kristie Young; William F. Maragos

doi:10.1016/j.nbd.2006.05.005

Inhibition of tumor necrosis factor-alpha signaling prevents human immunodeficiency virus-1 protein Tat and methamphetamine interaction

Shaji Theodore, Wayne A. Cass, Avindra Nath, Joseph Steiner, Kristie Young, William F. Maragos

Neuroscience

Research output: Contribution to journal › Article › peer-review

32 Scopus citations

Abstract

Our previous studies demonstrated that the psychostimulant methamphetamine (MA) and the human immunodeficiency virus-1 (HIV-1) protein Tat interacted to cause enhanced dopaminergic neurotoxicity. The present study examined whether tumor necrosis factor-alpha (TNF-α) mediates the interaction between Tat and MA. In Sprague-Dawley rats, injections of Tat caused a small but significant increase in striatal TNF-α level, whereas MA resulted in no change. The increase in TNF-α induced by Tat + MA was not significantly different from that induced by Tat alone. Temporal analysis of TNF-α levels revealed a 50-fold increase 4 h after Tat administration. In C57BL/6 mice, Tat + MA induced a 50% decline in striatal dopamine levels, which was significantly attenuated in mice lacking both receptors for TNF-α. TNF-α synthesis inhibitors significantly attenuated Tat + MA neurotoxicity in hippocampal neuronal culture. The results suggest that Tat-induced elevation of TNF-α may predispose the dopaminergic terminals to subsequent damage by MA.

Original language	English
Pages (from-to)	663-668
Number of pages	6
Journal	Neurobiology of Disease
Volume	23
Issue number	3
DOIs	https://doi.org/10.1016/j.nbd.2006.05.005
State	Published - Sep 2006

Bibliographical note

Funding Information:
This work was supported by grants DA13144 to WFM and AG17963 to WAC. The authors wish to thank Dr. Annadora Bruce-Keller (Department of Anatomy and Neurobiology, University of Kentucky) for providing TNF receptor knockout mice for the studies and Gary Pattison for technical assistance.

Funding

This work was supported by grants DA13144 to WFM and AG17963 to WAC. The authors wish to thank Dr. Annadora Bruce-Keller (Department of Anatomy and Neurobiology, University of Kentucky) for providing TNF receptor knockout mice for the studies and Gary Pattison for technical assistance.

Funders	Funder number
National Institute on Aging	R01AG017963

Keywords

AIDS
Basal ganglia
Cytokines
Dopamine
Drug abuse
Neurodegeneration

ASJC Scopus subject areas

Neurology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.nbd.2006.05.005

Cite this

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title = "Inhibition of tumor necrosis factor-alpha signaling prevents human immunodeficiency virus-1 protein Tat and methamphetamine interaction",

abstract = "Our previous studies demonstrated that the psychostimulant methamphetamine (MA) and the human immunodeficiency virus-1 (HIV-1) protein Tat interacted to cause enhanced dopaminergic neurotoxicity. The present study examined whether tumor necrosis factor-alpha (TNF-α) mediates the interaction between Tat and MA. In Sprague-Dawley rats, injections of Tat caused a small but significant increase in striatal TNF-α level, whereas MA resulted in no change. The increase in TNF-α induced by Tat + MA was not significantly different from that induced by Tat alone. Temporal analysis of TNF-α levels revealed a 50-fold increase 4 h after Tat administration. In C57BL/6 mice, Tat + MA induced a 50\% decline in striatal dopamine levels, which was significantly attenuated in mice lacking both receptors for TNF-α. TNF-α synthesis inhibitors significantly attenuated Tat + MA neurotoxicity in hippocampal neuronal culture. The results suggest that Tat-induced elevation of TNF-α may predispose the dopaminergic terminals to subsequent damage by MA.",

keywords = "AIDS, Basal ganglia, Cytokines, Dopamine, Drug abuse, Neurodegeneration",

author = "Shaji Theodore and Cass, \{Wayne A.\} and Avindra Nath and Joseph Steiner and Kristie Young and Maragos, \{William F.\}",

note = "Funding Information: This work was supported by grants DA13144 to WFM and AG17963 to WAC. The authors wish to thank Dr. Annadora Bruce-Keller (Department of Anatomy and Neurobiology, University of Kentucky) for providing TNF receptor knockout mice for the studies and Gary Pattison for technical assistance. ",

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AU - Theodore, Shaji

AU - Cass, Wayne A.

AU - Nath, Avindra

AU - Steiner, Joseph

AU - Young, Kristie

AU - Maragos, William F.

N1 - Funding Information: This work was supported by grants DA13144 to WFM and AG17963 to WAC. The authors wish to thank Dr. Annadora Bruce-Keller (Department of Anatomy and Neurobiology, University of Kentucky) for providing TNF receptor knockout mice for the studies and Gary Pattison for technical assistance.

PY - 2006/9

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N2 - Our previous studies demonstrated that the psychostimulant methamphetamine (MA) and the human immunodeficiency virus-1 (HIV-1) protein Tat interacted to cause enhanced dopaminergic neurotoxicity. The present study examined whether tumor necrosis factor-alpha (TNF-α) mediates the interaction between Tat and MA. In Sprague-Dawley rats, injections of Tat caused a small but significant increase in striatal TNF-α level, whereas MA resulted in no change. The increase in TNF-α induced by Tat + MA was not significantly different from that induced by Tat alone. Temporal analysis of TNF-α levels revealed a 50-fold increase 4 h after Tat administration. In C57BL/6 mice, Tat + MA induced a 50% decline in striatal dopamine levels, which was significantly attenuated in mice lacking both receptors for TNF-α. TNF-α synthesis inhibitors significantly attenuated Tat + MA neurotoxicity in hippocampal neuronal culture. The results suggest that Tat-induced elevation of TNF-α may predispose the dopaminergic terminals to subsequent damage by MA.

AB - Our previous studies demonstrated that the psychostimulant methamphetamine (MA) and the human immunodeficiency virus-1 (HIV-1) protein Tat interacted to cause enhanced dopaminergic neurotoxicity. The present study examined whether tumor necrosis factor-alpha (TNF-α) mediates the interaction between Tat and MA. In Sprague-Dawley rats, injections of Tat caused a small but significant increase in striatal TNF-α level, whereas MA resulted in no change. The increase in TNF-α induced by Tat + MA was not significantly different from that induced by Tat alone. Temporal analysis of TNF-α levels revealed a 50-fold increase 4 h after Tat administration. In C57BL/6 mice, Tat + MA induced a 50% decline in striatal dopamine levels, which was significantly attenuated in mice lacking both receptors for TNF-α. TNF-α synthesis inhibitors significantly attenuated Tat + MA neurotoxicity in hippocampal neuronal culture. The results suggest that Tat-induced elevation of TNF-α may predispose the dopaminergic terminals to subsequent damage by MA.

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KW - Basal ganglia

KW - Cytokines

KW - Dopamine

KW - Drug abuse

KW - Neurodegeneration

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Inhibition of tumor necrosis factor-alpha signaling prevents human immunodeficiency virus-1 protein Tat and methamphetamine interaction

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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