ABERRANT NEURITES AND SYNAPTIC VESICLE PROTEIN-DEFICIENCY IN SYNAPSIN II-DEPLETED NEURONS

被引:103
作者
FERREIRA, A
KOSIK, KS
GREENGARD, P
HAN, HQ
机构
[1] ROCKEFELLER UNIV,MOLEC & CELLULAR NEUROSCI LAB,NEW YORK,NY 10021
[2] HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR NEUROL DIS,BOSTON,MA 02115
关键词
D O I
10.1126/science.8178158
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
Synapsin I and synapsin II are neuron-specific phosphoproteins that have a role in the regulation of neurotransmitter release and in the formation of nerve terminals. After depletion of synapsin II by antisense oligonucleotides, rat hippocampal neurons in culture were unable to consolidate their minor processes and did not elongate axons. These aberrant morphological changes were accompanied by an abnormal distribution of intracellular filamentous actin (F-actin). In addition, synapsin II suppression resulted in a selective decrease in the amounts of several synaptic vesicle-associated proteins. These data suggest that synapsin II participates in cytoskeletal organization during the early stages of nerve cell development.
引用
收藏
页码:977 / 979
页数:3
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