Motorneurons Require Cysteine String Protein-¦Á to Maintain the Readily Releasable Vesicular Pool and Synaptic Vesicle Recycling

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• 作者：José ;   ; Luis Rozas¹ ; ^jrozas@us.es ; Leonardo Gó ; mez-Sá ; nchez¹ ; ⁴ ; Josif Mircheski¹ ; ⁴ ; Pedro Linares-Clemente¹ ; José ;   ; Luis Nieto-Gonzá ; lez¹ ; M.  ; Eugenio Vá ; zquez² ; Rafael Lujá ; n³ ; Rafael Ferná ; ndez-Chacó ; n¹ ; ^{rfchacon@us.es}
• 刊名：Neuron
• 出版年：2012
• 出版时间：12 April, 2012
• 年：2012
• 卷：74
• 期：1
• 页码：151-165
• 全文大小：2363 K

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Summary

Cysteine string protein-¦Á (CSP-¦Á) is a synaptic vesicle protein that prevents activity-dependent neurodegeneration by poorly understood mechanisms. We have studied the synaptic vesicle cycle at the motor nerve terminals of CSP-¦Á knock-out mice expressing the synaptopHluorin transgene. Mutant nerve terminals fail to sustain prolonged release and the number of vesicles available to be released decreases. Strikingly, the SNARE protein SNAP-25 is dramatically reduced. In addition, endocytosis during the stimulus fails to maintain the size of the recycling synaptic vesicle pool during prolonged stimulation. Upon depolarization, the styryl dye FM?2-10 becomes trapped and poorly releasable. Consistently with the functional results, electron microscopy analysis revealed characteristic features of impaired synaptic vesicle recycling. The unexpected defect in vesicle recycling in CSP-¦Á knock-out mice provides insights into understanding molecular mechanisms of degeneration in motor nerve terminals.