دانلود رایگان مقاله لاتین تغییر انتشار گلوتامات از سایت الزویر
عنوان فارسی مقاله:
تغییر انتشار گلوتامات در جسم مخطط پشتی بیماری پارکینسون مدل موش MitoPark
عنوان انگلیسی مقاله:
Altered glutamate release in the dorsal striatum of the MitoPark mouse model of Parkinson's disease
سال انتشار : 2016
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مقدمه انگلیسی مقاله:
1. Introduction
Mitochondrial dysfunction has been implicated in the degeneration of substantia nigra dopamine (SN-DA) neurons, which leads to behavioral impairments and ultimately Parkinson's disease (PD; Greenamyre and Hastings; 2004). Toxin and genetic models traditionally used to mimic PD demonstrated altered mitochondrial function as well as generation of PD-related behaviors and pathology (Dawson et al., 2010; Duty and Jenner, 2011). Recently, to better understand the role of mitochondrial dysfunction on the degeneration of the SN-DA neurons, a genetic mouse model was created in which mitochondrial function was disrupted in SNDA neurons by the knockout of the nuclear genome-encoded mitochondrial Tfam gene (Larsson et al., 1998). These mice, coined MitoPark mice, develop severe mitochondrial respiratory chain deficiencies in SN-DA neurons, which ultimately lead to the progressive degeneration, as well as the PD-associated behavioral deficits (Good et al., 2011). The MitoPark mice mimic the progression of PD in humans, with adult onset and slow progression of neurological symptoms (Ekstrand et al., 2007). The mouse phenotype includes a uniform and progressive loss of DA afferents in areas of the basal ganglia., The nigrostriatal DAergic projections innervating the dorsal striatum are strongly affected, while the mesolimbic projections which innervate the ventral striatum are spared (Ekstrand et al., 2007; Galter et al., 2010). The DAergic loss observed in MitoPark mice occurs over weeks to months, a more physiological model than the time course of days which is seen in toxin-induced models of PD, thus allowing for better understanding of mechanisms involved with PD pathology and progression. Due to the slow progression of disease in these mice, they make for a better tool to understand treatment strategies for PD. For example, previous studies have demonstrated that MitoPark mice are responsive to L-Dopa therapy with a differential response depending on disease state (Galter et al., 2010; Gellhaar et al., 2015). In addition, Shan et al.
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کلمات کلیدی:
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