Disease relevance of MPTP Poisoning

• Neurons containing norepinephrine in the brain are involved in the degenerative process of Parkinson's disease, whereas they are spared in MPTP-induced parkinsonism [1].

High impact information on MPTP Poisoning

• Pargyline prevents MPTP-induced parkinsonism in primates [2].
• Saccade responses to dopamine in human MPTP-induced parkinsonism [3].
• These influences of PARP-1 on p53 may underlie the mechanisms of MPTP-induced parkinsonism and other models of neuronal death [4].
• A novel in vivo post-translational modification of p53 by PARP-1 in MPTP-induced parkinsonism [4].
• The antioxidant OPC-14117 did not protect against MPTP-induced parkinsonism [5].

Chemical compound and disease context of MPTP Poisoning

• Effects of catechol-O-methyltransferase inhibition on the rates of uptake and reversibility of 6-fluoro-L-Dopa trapping in MPTP-induced parkinsonism in monkeys [6].
• MPTP-induced parkinsonism: acceleration of biochemical and behavioral recovery by GM1 ganglioside treatment [7].
• Effect of the NMDA antagonist MK-801 on MPTP-induced parkinsonism in the monkey [8].
• Monoamine oxidase B (MAO B) plays a pivotal role in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced Parkinsonism. An increased MAO B activity in platelets of patients with idiopathic Parkinson's disease (PD) is reported in this study [9].
• CONCLUSIONS: Chemopallidotomy using kainic acid permanently reversed the stigmata of MPTP-induced parkinsonism [10].

Anatomical context of MPTP Poisoning

• Effects of dopamine agonists on the spontaneous activity of globus pallidus neurons in monkeys with MPTP-induced parkinsonism [11].
• In cats recovered from MPTP-induced parkinsonism, a greater amount of dopamine was recovered from the extracellular fluid in the dorsolateral caudate following stimulated release of dopamine from the ventromedial striatum than after stimulated release locally in the dorsolateral caudate [12].

Gene context of MPTP Poisoning

• These results demonstrated that neuronal death occurred not only in SN but also in the SC of MPTP-treated mice and has provided evidence for a possible calpain-mediated SC neuronal death in MPTP-induced parkinsonism in mice [13].
• In conclusion, modulation of the astroglial antioxidant defense system might be one of the mechanisms by which Epo exerts a beneficial effect in MPTP-induced Parkinsonism [14].
• Reduced 125I-meta-iodobenzylguanidine uptake and norepinephrine transporter density in the hearts of mice with MPTP-induced parkinsonism [15].
• As the neuronal degeneration in MPTP-induced parkinsonism is thought to be caused by the inhibition of the mitochondrial respiration by 1-methyl-4-phenylpyridinium ion (MPP+), we studied the effects of TIQ-like alkaloids including dopamine-derived ones on the mitochondrial respiration using mouse brains [16].
• Monoamine-oxidase B (MAO-B) has been reported to be implicated in both MPTP-induced parkinsonism and Parkinson's disease, since selegiline (L-deprenyl), an irreversible MAO-B inhibitor, prevents MPTP-induced neurotoxicity in numerous species including mice, goldfish and drosophyla [17].

Analytical, diagnostic and therapeutic context of MPTP Poisoning

• Further investigations into the pathophysiology of MPTP-induced parkinsonism in the primate: an intracerebral microdialysis study of gamma-aminobutyric acid in the lateral segment of the globus pallidus [18].

References