PMID- 14999072
OWN - NLM
STAT- MEDLINE
DCOM- 20040514
LR  - 20221029
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 24
IP  - 9
DP  - 2004 Mar 3
TI  - Role of tumor necrosis factor-alpha in methamphetamine-induced drug dependence 
      and neurotoxicity.
PG  - 2212-25
AB  - Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is now 
      emerging as an important modulator of the function of the CNS. Methamphetamine 
      (METH) is a widely abused psychostimulant that causes euphoria, hyperactivity, 
      and drug dependence. High doses of METH cause long-term neurotoxicity in 
      dopaminergic neurons. In this study, we investigated a role of TNF-alpha in 
      METH-induced dependence and neurotoxicity. Repeated treatment with METH (2 mg/kg 
      for 5 d) in rats induced a significant increase in TNF-alpha mRNA and protein 
      expression in the brain. Exogenous TNF-alpha (1-4 microg) 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-alpha in behavioral and neurochemical effects of 
      METH, we used mice with targeted deletions of the TNF-alpha gene. TNF-alpha-(-/-) 
      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-alpha in METH-induced dopamine (DA) release and uptake in vitro and 
      in vivo in C57BL/6 mice. Exogenous TNF-alpha (4 microg) attenuated the 
      METH-induced increase in extracellular striatal DA in vivo and potentiated 
      striatal DA uptake into synaptosomes in vitro and in vivo. Furthermore, TNF-alpha 
      activated vesicular DA uptake by itself and diminished the METH-induced decrease 
      in vesicular DA uptake. Our findings suggest that TNF-alpha 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.
FAU - Nakajima, Akira
AU  - Nakajima A
AD  - Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University 
      Graduate School of Medicine, Nagoya 466-8560, Japan.
FAU - Yamada, Kiyofumi
AU  - Yamada K
FAU - Nagai, Taku
AU  - Nagai T
FAU - Uchiyama, Takehisa
AU  - Uchiyama T
FAU - Miyamoto, Yoshiaki
AU  - Miyamoto Y
FAU - Mamiya, Takayoshi
AU  - Mamiya T
FAU - He, Jue
AU  - He J
FAU - Nitta, Atsumi
AU  - Nitta A
FAU - Mizuno, Makoto
AU  - Mizuno M
FAU - Tran, Manh Hung
AU  - Tran MH
FAU - Seto, Aika
AU  - Seto A
FAU - Yoshimura, Masako
AU  - Yoshimura M
FAU - Kitaichi, Kiyoyuki
AU  - Kitaichi K
FAU - Hasegawa, Takaaki
AU  - Hasegawa T
FAU - Saito, Kuniaki
AU  - Saito K
FAU - Yamada, Yasuhiro
AU  - Yamada Y
FAU - Seishima, Mitsuru
AU  - Seishima M
FAU - Sekikawa, Kenji
AU  - Sekikawa K
FAU - Kim, Hyoung-Chun
AU  - Kim HC
FAU - Nabeshima, Toshitaka
AU  - Nabeshima T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Antigens, CD)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 44RAL3456C (Methamphetamine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Antigens, CD/genetics
MH  - Corpus Striatum/drug effects/metabolism
MH  - Discrimination Learning/drug effects/physiology
MH  - Disease Models, Animal
MH  - Dopamine/metabolism/pharmacokinetics
MH  - Male
MH  - Methamphetamine/*pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Microdialysis
MH  - Microinjections
MH  - Motor Activity/drug effects/genetics
MH  - Neurotoxicity Syndromes/*metabolism
MH  - Nucleus Accumbens/drug effects/physiology
MH  - Proto-Oncogene Proteins c-fos/biosynthesis
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Rats, Wistar
MH  - Receptors, Tumor Necrosis Factor/genetics
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Reward
MH  - Spatial Behavior/drug effects/physiology
MH  - Substance-Related Disorders/*metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/pharmacology/*physiology
PMC - PMC6730419
EDAT- 2004/03/06 05:00
MHDA- 2004/05/15 05:00
PMCR- 2004/09/03
CRDT- 2004/03/06 05:00
PHST- 2004/03/06 05:00 [pubmed]
PHST- 2004/05/15 05:00 [medline]
PHST- 2004/03/06 05:00 [entrez]
PHST- 2004/09/03 00:00 [pmc-release]
AID - 24/9/2212 [pii]
AID - 10.1523/JNEUROSCI.4847-03.2004 [doi]
PST - ppublish
SO  - J Neurosci. 2004 Mar 3;24(9):2212-25. doi: 10.1523/JNEUROSCI.4847-03.2004.