Depletion of cardiac norepinephrine in rats and mice by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
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Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by α-synuclein
2010, Neurobiology of DiseaseCitation Excerpt :It has been shown in three independently generated mouse null strains that a complete deficiency in α-SYN results in an attenuated DA depletion in response to MPTP intoxication in vivo, suggesting a genetic influence in the susceptibility to environmental insults (Dauer et al., 2002; Schluter et al., 2003; Drolet et al., 2004; Robertson et al., 2004; Klivenyi et al., 2006). MPTP/MPP+ administration can also cause the destruction of peripheral noradrenergic nerve terminals along with a reduction in cardiac accumulation of radiolabeled MIBG, and in NA recovery from myocardial tissue in rodents (Fukumitsu et al., 1984; Wallace et al., 1984; Fuller et al., 1984; Luthman and Jonsson, 1986; Fuller and Hemrick-Luecke, 1986; Algeri et al., 1987; Fuller et al., 1988; Ambrosio et al., 1988; Luthman and Sundstrom, 1990). Although previous analyses in α-syn knockout mice revealed that the PNS develops normally in these animals, the vulnerability of sympathetic neurons to noxious stimuli, including PD mimetic neurotoxins, has not been analyzed.
The MPTP Mouse Model of Parkinson's Disease: The True, the False, and the Unknown
2008, Parkinson's DiseaseThe MPTP Mouse Model of Parkinson's Disease: the True, the False, and the Unknown
2008, Parkinson's Disease: Molecular and Therapeutic Insights From Model Systems