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突触可塑性的结构和功能成分的遗传学剖析。II. 成束蛋白II控制突触前结构可塑性。

Genetic dissection of structural and functional components of synaptic plasticity. II. Fasciclin II controls presynaptic structural plasticity.

作者信息

Schuster C M, Davis G W, Fetter R D, Goodman C S

机构信息

Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.

出版信息

Neuron. 1996 Oct;17(4):655-67. doi: 10.1016/s0896-6273(00)80198-1.

DOI:10.1016/s0896-6273(00)80198-1
PMID:8893023
Abstract

Increased neuronal activity (eag Shaker mutants) and cAMP concentration (dunce mutants) lead to increased synaptic structure and function at the Drosophila neuromuscular junction. Here, we show that the increase in synaptic growth is accompanied by an approximately 50% decrease in synaptic levels of the cell adhesion molecule Fasciclin II (Fas II). This decrease in Fas II is both necessary and sufficient for presynaptic sprouting; FasII mutants that decrease Fas II levels by approximately 50% lead to sprouting similar to eag Shaker and dunce, while transgenes that maintain synaptic Fas II levels suppress sprouting in eag Shaker and dunce. However, FasII mutants that cause a 50% increase in bouton number do not alter synaptic strength; rather, evoked release from single boutons has a reduced quantal content, suggesting that the wild-type amount of release machinery is distributed throughout more boutons.

摘要

神经元活动增加(eag Shaker突变体)和环磷酸腺苷(cAMP)浓度升高(dunce突变体)会导致果蝇神经肌肉接头处的突触结构和功能增强。在此,我们表明突触生长的增加伴随着细胞黏附分子Fasciclin II(Fas II)的突触水平下降约50%。Fas II的这种下降对于突触前芽生既是必要的也是充分的;Fas II水平下降约50%的FasII突变体导致的芽生类似于eag Shaker和dunce突变体,而维持突触Fas II水平的转基因则抑制eag Shaker和dunce突变体中的芽生。然而,导致突触小体数量增加50%的FasII突变体并不会改变突触强度;相反,单个突触小体诱发的释放具有降低的量子含量,这表明野生型释放机制的量分布在更多的突触小体中。

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