Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system

被引:146
作者
Takei, Y
Harada, A
Takeda, S
Kobayashi, K
Terada, S
Noda, T
Takahashi, T
Hirokawa, N
机构
[1] UNIV TOKYO,SCH MED,DEPT ANAT & CELL BIOL,BUNKYO KU,TOKYO 113,JAPAN
[2] UNIV TOKYO,INST BRAIN RES,DEPT NEUROANAT,BUNKYO KU,TOKYO 113,JAPAN
[3] UNIV TOKYO,FAC MED,INST BRAIN RES,DEPT NEUROPHYSIOL,BUNKYO KU,TOKYO 113,JAPAN
[4] UNIV TOKYO,FAC PHARMACEUT SCI,DEPT NEUROBIOL & NEUROPATHOL,BUNKYO KU,TOKYO 113,JAPAN
[5] CANC INST,DEPT CELL BIOL,TOSHIMA KU,TOKYO 170,JAPAN
关键词
D O I
10.1083/jcb.131.6.1789
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of messy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the messy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure.
引用
收藏
页码:1789 / 1800
页数:12
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