Transmitter release deficits at the neuromuscular synapse of mice with mutations in the Cav2.1 (α1A) subunit of the P/Q-type Ca2+ channel

被引：7

作者：

Plomp, JJ

Van Den Maagdenberg, AM

Ferrari, MD

Frants, RR

Molenaar, PC

机构：

[1] Leiden Univ, Med Ctr, Dept Neurophysiol, NL-2300 RC Leiden, Netherlands

[2] Leiden Univ, Med Ctr, Dept Neurol, NL-2300 RC Leiden, Netherlands

[3] Leiden Univ, Med Ctr, Dept Human & Clin Genet, NL-2300 RC Leiden, Netherlands

来源：

MYASTHENIA GRAVIS AND RELATED DISORDERS: BIOMCHEMICAL BASIS FOR DISEASE OF THE NEUROMUSCULAR JUNCTION | 2003年 / 998卷

关键词：

P/Q-type Ca2+ channel; neuromuscular junction (NMJ); mutation;

D O I：

10.1196/annals.1254.005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

引用

页码：29 / 32

页数：4

共 4 条

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[3]

Plomp J J, 2001, Curr Opin Investig Drugs, V2, P1250

[4] Abnormal transmitter release at neuromuscular junctions of mice carrying the tottering α1A Ca2+ channel mutation [J].

Plomp, JJ ;

Vergouwe, MN ;

Van den Maagdenberg, AM ;

Ferrari, MD ;

Frants, RR ;

Molenaar, PC .

BRAIN, 2000, 123 :463-471

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