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Neuroscience letters

Role of Drosophila calcium channel cacophony in dopaminergic neurodegeneration and neuroprotection.


PMID 25445363

Abstract

One of the most important questions in Parkinson's disease (PD) regards the selective vulnerability of a specific population of dopaminergic (DA) neurons. Recent reports identify Ca(2+) channel as a potential source of this vulnerability. This work uses a Drosophila primary neuronal cell culture system as an in vitro PD model to explore the role of Ca(2+) homeostasis in DA neurodegeneration and protection. Our data showed that the Ca(2+) chelator EGTA is neuroprotective against a PD toxin MPP(+) (40 μM). We also use the genetic tools available in Drosophila to manipulate Ca(2+) channel activity. DA neurons lacking functional Ca(2+) channels (i.e., cacophony mutant) are inherently protected against MPP(+) toxicity. Furthermore, overexpression of wild type Ca(2+) channels in DA neurons blocks the rescue effect of a D2 agonist quinpirole on DA neurodegeneration. Our findings support the idea that Ca(2+) is a source of vulnerability for DA neurons and that the modulation of Ca(2+) levels in DA neurons could be a potential neuroprotective treatment.