Methamphetamine-induced neurotoxicity in BALB/c, DBA/2N and C57BL/6N mice

Kita, Taizo; Paku, Shunchoru; Takahashi, Masahiro; Kubo, Kaoru; Wagner, George C.; Nakashima, Toshikatsu

doi:10.1016/s0028-3908(98)00106-3

Cited by 44 publications

(26 citation statements)

References 24 publications

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“…5A). In contrast, consistent with a previous report (Kita et al, 1998), this dose regimen of METH did not affect 5-HT levels (data not shown), suggesting that this dose regimen did not induce serotonergic neurotoxicity in C57BL/6 mice. Pretreatment with TNF-␣ (4 g, i.p.)…”

Section: Effects Of Tnf-␣ On Neurotoxicity Of High Doses Of Meth In Micesupporting

confidence: 93%

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Nakajima¹,

Yamada²,

Nagai³

et al. 2004

J. Neurosci.

163

155

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Section: Effects Of Tnf-␣ On Neurotoxicity Of High Doses Of Meth In Micesupporting

confidence: 93%

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Nakajima¹,

Yamada²,

Nagai³

et al. 2004

J. Neurosci.

163

155

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“…With genetically controlled inbred strains of mice, it is generally recognized that there are clear strain differences in some behavioral effects induced by abused drugs (19,20,22). Consistent with previous results, morphine, but not methamphetamine or amphetamine, induced hyperlocomotion in BALB / c mice (24 -26), whereas cocaine significantly attenuated locomotor activity.…”

Section: Discussionsupporting

confidence: 83%

“…Kita et al (22) noticed that the order of intensity in stereotypy induced by methamphetamine was BALB / c>DBA>C57BL. Relatively high dose of methamphetamine engendered self-injurious behavior in BALB / c mice as compared with other strains without affecting the locomotor activity (23) (personal communication).…”

Section: Introductionmentioning

confidence: 99%

Complicated Interaction Between Psychostimulants and Morphine in Expression of Phenotype of Behavior in the Dopaminergic System of BALB/c Mice

et al. 2007

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Abstract. It is believed that BALB / c mice appear to be less sensitive to the locomotor effects of abused drugs compared to other strains, and several behaviors induced by abused drugs depend on genetic factors. The present study was designed to investigate the effects of the interaction between psychostimulants and morphine on behavior in BALB / c mice. Morphine and cocaine induced hyperlocomotion and hypolocomotion, respectively, while methamphetamine did not affect locomotor activity and high doses of methamphetamine significantly increased self-injurious behavior. Cocaine or methamphetamine increased the effects of morphine on locomotor behavior. Haloperidol (a dopamine-receptor antagonist) attenuated the hyperlocomotion induced by the combination of cocaine or methamphetamine plus morphine. These results indicate that the synergistic effects of methamphetamine or cocaine and morphine on locomotor activity are mediated through enhancement of the dopaminergic system and that combinations of psychostimulants and morphine enhance the locomotor activity in BALB / c mice. On the other hand, morphine completely attenuated methamphetamine-induced self-injurious behavior. Furthermore, a low dose (0.01 mg / kg) of haloperidol significantly increased the effects of methamphetamine and morphine on the locomotor activity. Hyperlocomotion induced by psychostimulants is mediated by the mesolimbic dopaminergic system, whereas stereotyped behaviors is mediated by the nigrostriatal dopaminergic system. Our findings suggest that balances of the activation of dopaminergic neurons (between mesolimbic and nigrostriatal systems) may play an important role to engender corresponding behavioral outcomes in BALB / c mice.

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“…Methamphetamine (METH) intoxication in mice produces neurodegeneration of dopaminergic terminals in the striatum and cell body loss in the substantia nigra pars compacta (SNpc) (Sonsalla et al, 1996;Hirata and Cadet, 1997;Kita et al, 1998). METH enters nerve terminals via the dopamine transporter (DAT) and displaces both vesicular and intracellular dopamine (DA).…”

mentioning

confidence: 99%

A New Poly(ADP-Ribose) Polymerase Inhibitor, FR261529 [2-(4-Chlorophenyl)-5-quinoxalinecarboxamide], Ameliorates Methamphetamine-Induced Dopaminergic Neurotoxicity in Mice

Iwashita¹,

Mihara²,

Yamazaki³

et al. 2004

J Pharmacol Exp Ther

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Methamphetamine (METH) administration in mice, results in a chronic dopamine (DA) depletion associated with nerve terminal damage, with DA oxidation and generation of reactive oxygen species (ROS) primarily mediating this neurotoxicity. The oxidative stress induced by METH putatively activates nuclear enzyme poly(ADPribose) polymerase (PARP), with excessive PARP activation eventually leading to cell death. In this study, we show that prevention of PARP activation by treatment with FR261529 [2-(4-chlorophenyl)-5-quinoxalinecarboxamide], the compound that was recently identified as a novel PARP inhibitor (IC 50 for PARP-1 ϭ 33 nM, IC 50 for PARP-2 ϭ 7 nM), protects against both ROS-induced cells injury in vitro and METH-induced dopaminergic neuronal damage in an in vivo Parkinson's disease (PD) model. In PC12 cells, exposure of hydrogen peroxide or METH markedly induced PARP activation, and treatment with FR261529 (1 M) significantly reduced PARP activation and attenuated cell death. In the mouse METH model, METH (15 mg/ kg ϫ 2 i.p., 2 h apart) intoxication accelerated DA metabolism and oxidation in the striatum, with subsequent cell damage in nigrostriatal dopaminergic neurons after 4 days. Oral administration of FR261529 (10 or 32 mg/kg) attenuated the damage of dopaminergic neurons via marked reduction of PARP activity and not via changes in dopamine metabolism or body temperature. These findings indicate that the neuroprotective effects of a novel PARP inhibitor, FR261529, were accompanied by inhibition of METH-induced PARP activation, suggesting that METH induces nigrostriatal dopaminergic neurodegeneration involving PARP activation and also orally active and brainpenetrable PARP inhibitor FR261529 could be a novel attractive therapeutic candidate for neurodegenerative disorders such as PD.

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Methamphetamine-induced neurotoxicity in BALB/c, DBA/2N and C57BL/6N mice

Cited by 44 publications

References 24 publications

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Complicated Interaction Between Psychostimulants and Morphine in Expression of Phenotype of Behavior in the Dopaminergic System of BALB/c Mice

A New Poly(ADP-Ribose) Polymerase Inhibitor, FR261529 [2-(4-Chlorophenyl)-5-quinoxalinecarboxamide], Ameliorates Methamphetamine-Induced Dopaminergic Neurotoxicity in Mice

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