Alpha-synuclein potentiates Ca2+ influx through voltage-dependent Ca2+ channels

被引：63

作者：

Adamczyk, Agata ^{[1
]}

Strosznajder, Joanna B. ^{[1
]}

机构：

[1] Polish Acad Sci, Med Res Ctr, Dept Cellular Signaling, PL-02106 Warsaw, Poland

来源：

NEUROREPORT | 2006年 / 17卷 / 18期

关键词：

alpha-synuclein; Ca2+ influx; synaptoneurosomes; voltage-dependent Ca2+ channels;

D O I：

10.1097/WNR.0b013e3280115185

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alpha-synuclein localized in synaptic terminals plays an important role in the pathogenesis of neurodegenerative diseases. The central domain of the protein, the nonamyloid component, is probably responsible for a-synuclein toxicity. Here, we report that a-synuclein and its nonamyloid component induced Ca2+ influx in rat synaptoneurosomes. The effect of alpha-synuclein was eliminated by the N-type specific Ca2+ channel blocker, omega-conotoxin GVIA. The antioxidant, resveratrol, and the nitric oxide synthase inhibitor, N-omega-nitro-L-arginine, did not prevent alpha-synuclein-incluced Ca2+ influx. Our findings indicate that a-synuclein stimulated Ca2+ influx through N-type voltage-dependent Ca2+ channels by a mechanism other than free radicals. A direct interaction between a-synuclein and N-type Ca2+ channels could be responsible for their effects on Ca2+ influx through voltage-dependent Ca2+ channels.

引用

页码：1883 / 1886

页数：4

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