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Abstract
Mitochondria are dynamic organelles that mediate the energetic supply to cells and mitigate oxidative stress through the intricate balance of fission and fusion. Mitochondrial dysfunction is a prominent feature within Parkinson disease (PD) etiologies. To date, there have been conflicting studies of neurotoxin impact on dopaminergic cell death, mitochondrial function and behavioral impairment using adult zebrafish. Here, we performed cerebroventricular microinjections (CVMIs) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on adult transgenic zebrafish that resulted in significant reductions in dopaminergic neurons within the telencephalon and olfactory bulbs (OB) of Tg(dat:eGFP) fish. Visualization of mCherry and mitochondrial gene expression analysis in Tg(dat:tom20 MLS:mCherry) fish reveal that MPTP induces mitochondrial fragmentation in dopaminergic neurons and the activation of the pink1/parkin pathway involved mitophagy. Moreover, the loss of dopaminergic neurons translated into a transient locomotor and olfactory phenotype. Taken together, these data can contribute to a better understanding of the mitochondrial impact on dopaminergic survivability.
Highlights
Idiopathic in nature, Parkinson disease (PD) is the second most prevalent neurodegenerative disease in the world where symptoms comprise of motor, sensory and cognitive impairments
Literature surrounding PD suffers from discrepancies among the degree of dopaminergic ablation and behavioral phenotypes resulting from neurotoxin treatments
We demonstrated that cerebroventricular microinjections (CVMIs) delivery of MPTP induces substantial dopaminergic neuron death within the telencephalon and olfactory regions of the adult zebrafish brain
Summary
Idiopathic in nature, Parkinson disease (PD) is the second most prevalent neurodegenerative disease in the world where symptoms comprise of motor, sensory and cognitive impairments (de Lau and Breteler, 2006; Muangpaisan et al, 2011). The pathology of PD has been characterized as a progressive loss of dopaminergic neurons within the substantia nigra of the human midbrain (Dauer and Przedborski, 2003; de Lau and Breteler, 2006; Muangpaisan et al, 2011). Motor and sensory symptoms develop following 40–60% loss of these neurons (Cheng et al, 2010). Researchers have elucidated mutations in various genes [PINK1 (Hatano et al, 2004), Parkin (Kitada et al, 1998; Dawson and Dawson, 2010), LRRK2 (Funayama et al, 2002; Zimprich et al, 2004), and DJ-1(Bonifati et al, 2003)] that increase an individual’s susceptibility to developing PD. This can only explain 5–10% of cases, while the majority are sporadically induced through external factors such as: age, gender, neurotoxic exposure, and mitochondrial dysfunction (Dexter and Jenner, 2013)
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