Spatial learning is unimpaired in mice containing a deletion of the alpha-synuclein locus

被引:32
作者
Chen, PE
Specht, CG
Morris, RGM
Schoepfer, R
机构
[1] UCL, Dept Pharmacol, Mol Pharmacol Lab, London WC1E 6BT, England
[2] Univ Edinburgh, Dept Neurosci, Edinburgh EH8 9JZ, Midlothian, Scotland
关键词
C57BL/6S; Del(6)Snca1Slab; Harlan; Snca;
D O I
10.1046/j.1460-9568.2002.02062.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
alpha-Synuclein belongs to a family of structurally related proteins expressed highly in the brain and is the major component of filamentous deposits present in a range of neurodegenerative diseases (synucleinopathies). It has been implicated in learning and memory, yet the physiological role of this protein is still unclear. It was recently found that a subpopulation of C57BL/6J mice carries a chromosomal deletion of the alpha-synuclein locus, often unknown to the experimenter. As genetically engineered mice are often backcrossed with C57BL/6J animals for learning and memory experiments, we studied the importance of alpha-synuclein in spatial learning tasks by examining the performance of alpha-synuclein(-/-) mice in the hidden platform reference memory version of the watermaze. Our data show that alpha-synuclein(-/-) mice had no significant impairment in performance during training or probe trials, compared with wild-type littermates. Therefore, we conclude that alpha-synuclein is not essential for this type of spatial learning.
引用
收藏
页码:154 / 158
页数:5
相关论文
共 22 条
[1]   Mice lacking α-synuclein display functional deficits in the nigrostriatal dopamine system [J].
Abeliovich, A ;
Schmitz, Y ;
Fariñas, I ;
Choi-Lundberg, D ;
Ho, WH ;
Castillo, PE ;
Shinsky, N ;
Verdugo, JMG ;
Armanini, M ;
Ryan, A ;
Hynes, M ;
Phillips, H ;
Sulzer, D ;
Rosenthal, A .
NEURON, 2000, 25 (01) :239-252
[2]  
Clayton DF, 1999, J NEUROSCI RES, V58, P120, DOI 10.1002/(SICI)1097-4547(19991001)58:1<120::AID-JNR12>3.0.CO
[3]  
2-E
[4]   The synucleins: a family of proteins involved in synaptic function, plasticity, neurodegeneration and disease [J].
Clayton, DF ;
George, JM .
TRENDS IN NEUROSCIENCES, 1998, 21 (06) :249-254
[5]  
Duda JE, 2000, J NEUROSCI RES, V61, P121, DOI 10.1002/1097-4547(20000715)61:2<121::AID-JNR1>3.0.CO
[6]  
2-4
[7]   Synphilin-1 associates with α-synuclein and promotes the formation of cytosolic inclusions [J].
Engelender, S ;
Kaminsky, Z ;
Guo, X ;
Sharp, AH ;
Amaravi, RK ;
Kleiderlein, JJ ;
Margolis, RL ;
Troncoso, JC ;
Lanahan, AA ;
Worley, PF ;
Dawson, VL ;
Dawson, TM ;
Ross, CA .
NATURE GENETICS, 1999, 22 (01) :110-114
[8]   CHARACTERIZATION OF A NOVEL PROTEIN REGULATED DURING THE CRITICAL PERIOD FOR SONG LEARNING IN THE ZEBRA FINCH [J].
GEORGE, JM ;
JIN, H ;
WOODS, WS ;
CLAYTON, DF .
NEURON, 1995, 15 (02) :361-372
[9]   Alpha-synuclein and neurodegenerative diseases [J].
Goedert, M .
NATURE REVIEWS NEUROSCIENCE, 2001, 2 (07) :492-501
[10]   Regulation of phospholipase D2:: Selective inhibition of mammalian phospholipase D isoenzymes by α- and β-synucleins [J].
Jenco, JM ;
Rawlingson, A ;
Daniels, B ;
Morris, AJ .
BIOCHEMISTRY, 1998, 37 (14) :4901-4909