Zebrafish as a new animal model for movement disorders

被引：95

作者：

Flinn, Laura ^{[1
,2
]}

Bretaud, Sandrine ^{[3
]}

Lo, Christine ^{[1
,2
]}

Ingham, Phillip W. ^{[2
]}

Bandmann, Oliver ^{[1
,2
]}

机构：

[1] Univ Sheffield, Acad Neurol Unit, Sch Med, Sheffield S10 2RX, S Yorkshire, England

[2] Univ Sheffield, MRC, Ctr Dev & Biomed Genet, Sheffield S10 2RX, S Yorkshire, England

[3] Univ Lyon 1, Inst Biol & Chim Prot, F-69365 Lyon, France

来源：

JOURNAL OF NEUROCHEMISTRY | 2008年 / 106卷 / 05期

基金：

英国医学研究理事会;

关键词：

dopamine; Huntington's disease; movement disorders; Parkinson's disease; zebrafish;

D O I：

10.1111/j.1471-4159.2008.05463.x

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：

The zebrafish, long recognized as a model organism for the analysis of basic developmental processes, is now also emerging as an alternative animal model for human diseases. This review will first provide an overview of the particular characteristics of zebrafish in general and their dopaminergic nervous system in particular. We will then summarize all work undertaken so far to establish zebrafish as a new animal model for movement disorders and will finally emphasize its particular strength - amenability to high throughput in vivo drug screening.

引用

页码：1991 / 1997

页数：7

共 39 条

[21] Huntingtin-deficient zebrafish exhibit defects in iron utilization and development [J].

Lumsden, Amanda L. ;

Henshall, Tanya L. ;

Dayan, Sonia ;

Lardelli, Michael T. ;

Richards, Robert I. .

HUMAN MOLECULAR GENETICS, 2007, 16 (16) :1905-1920

[22] Consistency in the number of dopaminergic paraventricular organ-accompanying neurons in the posterior tuberculum of the zebrafish brain [J].

Ma, PM ;

Lopez, M .

BRAIN RESEARCH, 2003, 967 (1-2) :267-272

[23] Neuroprotection of MPTP-induced toxicity in zebrafish dopaminergic neurons [J].

McKinley, ET ;

Baranowski, TC ;

Blavo, DO ;

Cato, C ;

Doan, TN ;

Rubinstein, AL .

MOLECULAR BRAIN RESEARCH, 2005, 141 (02) :128-137

[24] Knockdown of the survival motor neuron (Smn) protein in zebrafish causes defects in motor axon outgrowth and pathfinding [J].

McWhorter, ML ;

Monani, UR ;

Burghes, AHM ;

Beattie, CE .

JOURNAL OF CELL BIOLOGY, 2003, 162 (05) :919-931

[25] CHIP suppresses polyglutamine aggregation and toxicity in vitro and in vivo [J].

Miller, VM ;

Nelson, RF ;

Gouvion, CM ;

Williams, A ;

Rodriguez-Lebron, E ;

Harper, SQ ;

Davidson, BL ;

Rebagliati, MR ;

Paulson, HL .

JOURNAL OF NEUROSCIENCE, 2005, 25 (40) :9152-9161

[26] Effective targeted gene 'knockdown' in zebrafish [J].

Nasevicius, A ;

Ekker, SC .

NATURE GENETICS, 2000, 26 (02) :216-220

[27]

Parng Chuenlei, 2007, Journal of Pharmacological and Toxicological Methods, V55, P103, DOI 10.1016/j.vascn.2006.04.004

[28] A zebrafish assay for identifying neuroprotectants in vivo [J].

Parng, Chuenlei ;

Ton, Christopher ;

Lin, Ying-Xin ;

Roy, Nicole Marie ;

McGrath, Patricia .

NEUROTOXICOLOGY AND TERATOLOGY, 2006, 28 (04) :509-516

[29] Chemical suppression of a genetic mutation in a zebrafish model of aortic coarctation [J].

Peterson, RT ;

Shaw, SY ;

Peterson, TA ;

Milan, DJ ;

Zhong, TP ;

Schreiber, SL ;

MacRae, CA ;

Fishman, MC .

NATURE BIOTECHNOLOGY, 2004, 22 (05) :595-599

[30] The too few mutant selectively affects subgroups of monoaminergic neurons in the zebrafish forebrain [J].

Rink, E ;

Guo, S .

NEUROSCIENCE, 2004, 127 (01) :147-154

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