Research reportHistochemical, biochemical and behavioural consequences of MPTP treatment in C-57 black mice
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Phloretin attenuates behavior deficits and neuroinflammatory response in MPTP induced Parkinson's disease in mice
2019, Life SciencesCitation Excerpt :The pathologic conditions of PD can be created by MPTP administration in animals to make them as experimental PD models which exhibit odd behavioral changes and pathophysiological features of neurodegenerative disorders, including oxidative stress, dopaminergic neurodegeneration and neuroinflammation-mediated glial cell activation [24,25]. Previous studies also showed that the MPTP administration to rodents and primates induce DA neuron loss in SNpc and cause depleted a DA level which leads to severe motor dysfunction [26]. In the present study, we investigated the neuroprotective role of PHL in MPTP induced degeneration of dopaminergic neurons which is well elucidated through enhanced DA levels, improved behavioral impairments, inhibition of glial cell activation and suppression of inflammatory responses in the mice of experimental groups treated with PHL.
Hederagenin and α-hederin promote degradation of proteins in neurodegenerative diseases and improve motor deficits in MPTP-mice
2017, Pharmacological ResearchCitation Excerpt :For example, while there was literature reporting the long lasting motor deficit in mice after toxin administration [83,84], there were reports depicting the restoration of motor function [85]. It is also noted worthy that there were literatures reporting no changed or hyperactive locomotion in mice after MPTP injection [37,86]. In summary, by depicting the protective role of autophagy in facilitating the degradation of neurodegenerative disease proteins such as α-syn and huntingtin, our study has provided novel insight into the drug discovery of autophagic inducers from traditional Chinese medicinal plants, and suggested the possible molecular mechanisms and therapeutic role of the newly identified active components, hederagenin and α-hederin, from HH in modulating PD or HD.
Sustained resistance to acute MPTP toxicity by hypothalamic dopamine neurons following chronic neurotoxicant exposure is associated with sustained up-regulation of parkin protein
2013, NeuroToxicologyCitation Excerpt :Despite these differences in DA reuptake mechanisms, the cellular machinery responsible for DA synthesis, storage, release and catabolism are similar in both NSDA and TIDA neurons. The differential susceptibility of TIDA and NSDA neurons to PD-associated cellular pathology has also been observed in neurotoxicant-based animal models of PD (Willis and Donnan, 1987; Mogi et al., 1988; Sundstrum et al., 1990; Behrouz et al., 2007; Benskey et al., 2012). Despite inherent limitations, neurotoxicant-based models of PD accurately recapitulate many of the key molecular pathological features associated with PD, including mitochondrial dysfunction, oxidative stress, impairment of ubiquitin proteasome pathway (UPP) function, activation of programmed cell death, and neuroinflammation (Zang and Misra, 1993; Jackson-Lewis et al., 1995; Petroske et al., 2001; Dauer and Przedborski, 2003; Hoglinger et al., 2003; Przedborski et al., 2004; Fornai et al., 2005; Chan et al., 2006).
Neurotoxin-based models of Parkinson's disease
2012, NeuroscienceCitation Excerpt :The second important aspect is that, after recovering from the injections, mice look normal, meaning that highly challenging behavioral test are required to unravel some of the deficits they may display. Indeed, MPTP-intoxicated mice exhibit a remarkable capacity for functional recovery, for which reason some motor impairments are only transient in nature (Willis and Donnan, 1987; Sedelis et al., 2001). Finally, as motor impairment is correlated with the lesion magnitude, it is therefore more difficult to conduct behavioral tests in the case of moderate lesions of the dopaminergic system.