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rdf:type |
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lifeskim:mentions |
umls-concept:C0021051,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0025611,
umls-concept:C0033684,
umls-concept:C0037083,
umls-concept:C0086418,
umls-concept:C0961954,
umls-concept:C1100939,
umls-concept:C1292733,
umls-concept:C1456820,
umls-concept:C1704675,
umls-concept:C1710082
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pubmed:issue |
3
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pubmed:dateCreated |
2006-8-22
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pubmed:abstractText |
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-alpha) mediates the interaction between Tat and MA. In Sprague-Dawley rats, injections of Tat caused a small but significant increase in striatal TNF-alpha level, whereas MA resulted in no change. The increase in TNF-alpha induced by Tat + MA was not significantly different from that induced by Tat alone. Temporal analysis of TNF-alpha 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-alpha. TNF-alpha synthesis inhibitors significantly attenuated Tat + MA neurotoxicity in hippocampal neuronal culture. The results suggest that Tat-induced elevation of TNF-alpha may predispose the dopaminergic terminals to subsequent damage by MA.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0969-9961
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
663-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:16828290-AIDS Dementia Complex,
pubmed-meshheading:16828290-Amphetamine-Related Disorders,
pubmed-meshheading:16828290-Animals,
pubmed-meshheading:16828290-Basal Ganglia,
pubmed-meshheading:16828290-Cells, Cultured,
pubmed-meshheading:16828290-Disease Models, Animal,
pubmed-meshheading:16828290-Dopamine,
pubmed-meshheading:16828290-Dopamine Uptake Inhibitors,
pubmed-meshheading:16828290-Encephalitis,
pubmed-meshheading:16828290-Gene Products, tat,
pubmed-meshheading:16828290-Humans,
pubmed-meshheading:16828290-Male,
pubmed-meshheading:16828290-Methamphetamine,
pubmed-meshheading:16828290-Mice,
pubmed-meshheading:16828290-Mice, Inbred C57BL,
pubmed-meshheading:16828290-Mice, Knockout,
pubmed-meshheading:16828290-Oxidative Stress,
pubmed-meshheading:16828290-Presynaptic Terminals,
pubmed-meshheading:16828290-Protein Synthesis Inhibitors,
pubmed-meshheading:16828290-Rats,
pubmed-meshheading:16828290-Rats, Sprague-Dawley,
pubmed-meshheading:16828290-Tumor Necrosis Factor-alpha,
pubmed-meshheading:16828290-Up-Regulation,
pubmed-meshheading:16828290-tat Gene Products, Human Immunodeficiency Virus
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pubmed:year |
2006
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pubmed:articleTitle |
Inhibition of tumor necrosis factor-alpha signaling prevents human immunodeficiency virus-1 protein Tat and methamphetamine interaction.
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pubmed:affiliation |
Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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