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Role of Drosophila calcium channel cacophony in dopaminergic neurodegeneration and neuroprotection.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
2015 (English)In: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 584Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2015. Vol. 584
National Category
URN: urn:nbn:se:uu:diva-279698DOI: 10.1016/j.neulet.2014.11.004PubMedID: 25445363OAI: oai:DiVA.org:uu-279698DiVA: diva2:908679
Available from: 2016-03-03 Created: 2016-03-03 Last updated: 2016-03-03

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