Heterozygous VMAT2 knockout mice display prolonged QT intervals: possible contributions to sudden death

被引：19

作者：

Itokawa, K

Sora, I

Schindler, CW

Itokawa, M

Takahashi, N

Uhl, GR ^{[1
]}

机构：

[1] NIDA, Mol Neurobiol Branch, Intramural Res Program, Baltimore, MD 21224 USA

[2] NIDA, Preclin Pharmacol Sect, Intramural Res Program, Baltimore, MD 21224 USA

[3] Osaka Univ, Grad Sch Med, Dept Neurol, Suita, Osaka 5650871, Japan

[4] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21224 USA

[5] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21224 USA

来源：

MOLECULAR BRAIN RESEARCH | 1999年 / 71卷 / 02期

基金：

美国国家卫生研究院;

关键词：

vesicular monoamine transporter 2; transgenic mouse; electrocardiogram; telemetry; prolonged QT;

D O I：

10.1016/S0169-328X(99)00194-1

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Heterozygous knockout (KO) mice with half of wild-type levels of expression of the vesicular monoamine transporter (VMAT2) can suddenly die in midlife. To seek mechanisms for this sudden death, we have examined electrocardiogram (ECG) data telemetered from freely-moving heterozygote and wild-type littermate mice. Many ECG parameters were indistinguishable in mice of these two strains. However, heterozygous mice displayed prolonged QT intervals. These findings provide likely contributions to differences in vulnerability to lethal arrhythmias in these animals, and a candidate gene for contributions to human interindividual differences in vulnerability to cardiac arrhythmias. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：354 / 357

页数：4

共 14 条

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