IMPAIRMENT OF AXONAL DEVELOPMENT AND OF SYNAPTOGENESIS IN HIPPOCAMPAL-NEURONS OF SYNAPSIN I-DEFICIENT MICE
IMPAIRMENT OF AXONAL DEVELOPMENT AND OF SYNAPTOGENESIS IN HIPPOCAMPAL-NEURONS OF SYNAPSIN I-DEFICIENT MICE
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DOI：
10.1073/pnas.92.20.9230
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发表时间：
1995-09-26
影响因子：
11.1
通讯作者：
GREENGARD, P
中科院分区：
文献类型：
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作者：
CHIN, LS;LI, L;GREENGARD, P
突触蛋白 I 是所有神经元磷蛋白中最丰富的，在突触小泡中富含。据推测，突触蛋白 I 可以调节成体神经末梢的突触发生和神经递质释放。这些角色的证据具有很强的启发性，但并不令人信服。为了评估突触蛋白 I 在突触发生和成年突触功能中可能的参与，我们通过同源重组产生了突触蛋白 I 缺陷小鼠。我们在此报道，在胚胎突触蛋白I突变小鼠的海马神经元中，树突前神经突和轴突的生长严重延迟。此外，在这些突变神经元中突触形成显着延迟。这些结果表明突触蛋白 I 在轴突发生和突触发生的调节中发挥作用。
Synapsin I, the most abundant of all neuronal phosphoproteins, is enriched in synaptic vesicles, It has been hypothesized to regulate synaptogenesis and neurotransmitter release from adult nerve terminals. The evidence for such roles has been highly suggestive but not compelling. To evaluate the possible involvement of synapsin I in synaptogenesis and in the function of adult synapses, we have generated synapsin I-deficient mice by homologous recombination. We report herein that outgrowth of predendritic neurites and of axons was severely retarded in the hippocampal neurons of embryonic synapsin I mutant mice, Furthermore, synapse formation was significantly delayed in these mutant neurons. These results indicate that synapsin I plays a role in regulation of axonogenesis and synaptogenesis.