Increase in membrane surface expression and phosphorylation of TRPC3 related to olfactory dysfunction in α-synuclein transgenic mice.
Increase in membrane surface expression and phosphorylation of TRPC3 related to olfactory dysfunction in α-synuclein transgenic mice.
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DOI：
10.1111/jcmm.17524
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发表时间：
2022-10
影响因子：
5.3
通讯作者：
中科院分区：
文献类型：
--
作者：
Olfactory impairment is an initial non‐motor symptom of Parkinson's disease that causes the deposition of aggregated α‐synuclein (α‐syn) in olfactory neurons. Transient receptor potential canonical (TRPC) channels are a diverse group of non‐selective Ca2+ entry channels involved in the progression or pathogenesis of PD via Ca2+ homeostatic regulation. However, the relationship between TRPC and α‐syn pathology in an olfactory system remains unclear. To address this issue, we assessed the olfactory function in α‐syn transgenic mice. In contrast with control mice, the transgenic mice exhibited impaired olfaction, TRPC3 activation and apoptotic neuronal cell death in the olfactory system. Similar results were observed in primary cultures of olfactory neurons, that is TRPC3 activation, increasing intracellular Ca2+ concentration and apoptotic cell death in the α‐syn‐overexpressed neurons. These changes were significantly attenuated by TRPC3 knockdown. Therefore, our findings suggest that TRPC3 activation and calcium dyshomeostasis play a key role in α‐syn‐induced olfactory dysfunction in mice.
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影响因子：
12.7
作者：
Hoeglinger, Guenter U.;Alvarez-Fischer, Daniel;Oertel, Wolfgang H.
通讯作者：
Oertel, Wolfgang H.
DOI：
10.1111/j.1460-9568.2008.06346.x
发表时间：
2008-07
期刊：
The European journal of neuroscience
影响因子：
--
作者：
Fleming SM;Tetreault NA;Mulligan CK;Hutson CB;Masliah E;Chesselet MF
通讯作者：
Chesselet MF
影响因子：
4.8
作者：
Guo P;Wang RD;Lian TH;Ding DY;Zhang YN;Zhang WJ;Li DN;Li LX;Li JH;Guan HY;Yu SY;Liu L;Hu Y;Zuo LJ;Yu QJ;Wang XM;Zhang W
通讯作者：
Zhang W
影响因子：
3.5
作者：
Cederholm, Jennie M. E.;Kim, Youngsoo;Housley, Gary D.
通讯作者：
Housley, Gary D.
DOI：
10.1073/pnas.0508030102
发表时间：
2006-01-10
影响因子：
11.1
作者：
Kawasaki, BT;Liao, YH;Birnbaumer, L
通讯作者：
Birnbaumer, L