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In this study, we investigated a role of TNF-\u03b1 in METH-induced dependence and neurotoxicity. Repeated treatment with METH (2 mg\/kg for 5 d) in rats induced a significant increase in TNF-\u03b1 mRNA and protein expression in the brain. Exogenous TNF-\u03b1 (1-4 \u03bcg) blocked locomotor-stimulating and rewarding effects of METH, as well as METH (4 mg\/kg; four times at 2 hr intervals)-induced dopaminergic neurotoxicity in mice. To examine a role of endogenous TNF-\u03b1 in behavioral and neurochemical effects of METH, we used mice with targeted deletions of the TNF-\u03b1 gene. TNF-\u03b1-(-\/-) mice showed enhanced responses to the locomotor-sensitizing, rewarding, and neurotoxic effects of METH compared with wild-type mice. We also examined the role of TNF-\u03b1 in METH-induced dopamine (DA) release and uptake<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>in C57BL\/6 mice. Exogenous TNF-\u03b1 (4 \u03bcg) attenuated the METH-induced increase in extracellular striatal DA<jats:italic>in vivo<\/jats:italic>and potentiated striatal DA uptake into synaptosomes<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>. Furthermore, TNF-\u03b1 activated vesicular DA uptake by itself and diminished the METH-induced decrease in vesicular DA uptake. Our findings suggest that TNF-\u03b1 plays a neuroprotective role in METH-induced drug dependence and neurotoxicity by activating plasmalemmal and vesicular DA transporter as well as inhibiting METH-induced increase in extracellular DA levels.<\/jats:p>","DOI":"10.1523\/jneurosci.4847-03.2004","type":"journal-article","created":{"date-parts":[[2004,3,3]],"date-time":"2004-03-03T18:02:46Z","timestamp":1078336966000},"page":"2212-2225","source":"Crossref","is-referenced-by-count":161,"title":["Role of Tumor Necrosis Factor-\u03b1 in Methamphetamine-Induced Drug Dependence and 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