Synapsin I accelerates the kinetics of neurotransmitter release in mouse motor terminals.
Synapsin I accelerates the kinetics of neurotransmitter release in mouse motor terminals.
复制标题
突触蛋白 I 加速小鼠运动末梢神经递质释放的动力学。
DOI：
10.1002/syn.20635
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Bykhovskaia,Maria
中科院分区：
文献类型：
--
作者：
Coleman,WilliamL;Bykhovskaia,Maria
Synapsins are an abundant and highly conserved family of phosphoproteins associated with synaptic vesicles. In its dephosphorylated form, synapsin binds to synaptic vesicles and triggers actin polymerization (Greengard et al., 1993 for review; Han and Greengard, 1994), while synapsin phosphorylation causes its dissociation from vesicles and dispersion, thus allowing mobilization of synaptic vesicles for exocytosis (Hosaka et al., 1999; Murthy 2001; Chi et al., 2001, 2003; Cousin et al., 2003). Mice lacking one or several synapsin genes (I, II, or III) have reduced vesicle density and modified short-term plasticity (Rosahl et al., 1995; Gitler et al., 2004; Samigullin at al., 2004). Injections of synapsin E-domain into squid giant axon (Hilfiker et al., 1998) slowed down the kinetics of release, while overexpression of this domain accelerated the release kinetics (Fassio et al., 2006), suggesting that synapsin may affect the final stages of exocytosis. In support of this hypothesis, our study presents the first evidence of altered release kinetics in the nerve terminals of synapsin gene deleted animals.Mice homozygous for the Syn1tm1Sud and Syn2tm1Sud targeted mutation, synapsin I (-) and synapsin II (-), respectively, were purchased from The Jackson Laboratory (strains B6129S-Syn1tm1Sud/J and B6129S-Syn2tm1Sud/J). Strain B6129SF2/J (Jackson Laboratory) was used as a control (WT) to provide a genetic match to the synapsin I (-) and synapsin II (-) mice.
