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Methamphetamine protects against MPTP neurotoxicity in C57BL mice.

作者信息

Sziráki I, Kardos V, Patthy M, Pátfalusi M, Budai G

机构信息

Division of Biochemistry, Institute for Drug Research, Budapest, Hungary.

出版信息

Eur J Pharmacol. 1994 Jan 14;251(2-3):311-4. doi: 10.1016/0014-2999(94)90416-2.

DOI:10.1016/0014-2999(94)90416-2
PMID:8149986
Abstract

Methamphetamine (5 mg/kg) administered 30 min prior to each injection with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (3 x 30 mg/kg, at 24 h intervals) prevents the reduction of striatal levels of dopamine and its metabolites in C57BL mice. Methamphetamine and amphetamine inhibit the uptake of 1-methyl-4-phenylpyridinium (MPP+) by striatal synaptosomes of rats. A 30-min post-treatment with methamphetamine or amphetamine also prevents the MPTP-induced dopamine depletion, suggesting that their protective effect is related to the blockade of MPP+ uptake into dopaminergic neurons. Since amphetamine and methamphetamine are themselves neurotoxins at higher doses, this work demonstrated the protection against the actions of one neurotoxin by the administration of another.

摘要

相似文献

1
Methamphetamine protects against MPTP neurotoxicity in C57BL mice.
Eur J Pharmacol. 1994 Jan 14;251(2-3):311-4. doi: 10.1016/0014-2999(94)90416-2.
2
Striatal MPP+ levels do not necessarily correlate with striatal dopamine levels after MPTP treatment in mice.在小鼠经MPTP处理后,纹状体中MPP+水平不一定与纹状体多巴胺水平相关。
Neurodegeneration. 1996 Jun;5(2):129-36. doi: 10.1006/neur.1996.0019.
3
MK-801 temporarily prevents MPTP-induced acute dopamine depletion and MPP+ elimination in the mouse striatum.MK-801可暂时阻止小鼠纹状体内MPTP诱导的急性多巴胺耗竭及MPP+的清除。
J Pharmacol Exp Ther. 1993 Dec;267(3):1515-20.
4
Lowering ambient or core body temperature elevates striatal MPP+ levels and enhances toxicity to dopamine neurons in MPTP-treated mice.降低环境温度或核心体温会提高纹状体中MPP+的水平,并增强MPTP处理的小鼠中多巴胺神经元的毒性。
Brain Res. 1998 Apr 20;790(1-2):264-9. doi: 10.1016/s0006-8993(98)00069-9.
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Amphetamine-metabolites of deprenyl involved in protection against neurotoxicity induced by MPTP and 2'-methyl-MPTP.司来吉兰的苯丙胺代谢产物参与对MPTP和2'-甲基-MPTP诱导的神经毒性的保护作用。
J Neural Transm Suppl. 1994;41:207-19. doi: 10.1007/978-3-7091-9324-2_27.
6
Acute Restraint Stress Augments 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Neurotoxicity via Increased Toxin Uptake into the Brain in C57BL/6 Mice.急性束缚应激通过增加 C57BL/6 小鼠脑内毒素摄取增强 1-甲基-4-苯基-1,2,3,6-四氢吡啶神经毒性。
Neurosci Bull. 2018 Oct;34(5):849-853. doi: 10.1007/s12264-018-0254-2. Epub 2018 Jul 9.
7
Transgenic mice with increased Cu/Zn-superoxide dismutase activity are resistant to N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity.具有增强的铜/锌超氧化物歧化酶活性的转基因小鼠对N-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的神经毒性具有抗性。
J Neurosci. 1992 May;12(5):1658-67. doi: 10.1523/JNEUROSCI.12-05-01658.1992.
8
In brown Norway rats, MPP+ is accumulated in the nigrostriatal dopaminergic terminals but it is not neurotoxic: a model of natural resistance to MPTP toxicity.在棕色挪威大鼠中,MPP+在黑质纹状体多巴胺能终末中蓄积,但它没有神经毒性:一种对MPTP毒性天然抵抗的模型。
Exp Neurol. 1994 May;127(1):54-61. doi: 10.1006/exnr.1994.1079.
9
Effect of acetyl-L-carnitine on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity.乙酰左旋肉碱对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)神经毒性的影响。
Biochem Pharmacol. 1993 May 25;45(10):2170-2. doi: 10.1016/0006-2952(93)90034-t.
10
Effects of noradrenergic lesions on MPTP/MPP+ kinetics and MPTP-induced nigrostriatal dopamine depletions.去甲肾上腺素能损伤对MPTP/MPP+动力学及MPTP诱导的黑质纹状体多巴胺耗竭的影响。
J Pharmacol Exp Ther. 1997 Oct;283(1):100-7.

引用本文的文献

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Parkinson's disease: animal models and dopaminergic cell vulnerability.帕金森病:动物模型与多巴胺能细胞易损性
Front Neuroanat. 2014 Dec 15;8:155. doi: 10.3389/fnana.2014.00155. eCollection 2014.
2
Increased dopaminergic neuron sensitivity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in transgenic mice expressing mutant A53T alpha-synuclein.在表达突变型A53Tα-突触核蛋白的转基因小鼠中,多巴胺能神经元对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)的敏感性增加。
Neurochem Res. 2008 May;33(5):902-11. doi: 10.1007/s11064-007-9533-4. Epub 2007 Nov 13.
3
Metabolism of (-)-deprenyl and PF-(-)-deprenyl in brain after central and peripheral administration.
中枢和外周给药后,脑内(-)-司来吉兰和PF-(-)-司来吉兰的代谢。
Neurochem Res. 1996 Oct;21(10):1155-60. doi: 10.1007/BF02532389.