Reist N E, Buchanan J, Li J, DiAntonio A, Buxton E M, Schwarz T L
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523, USA.
J Neurosci. 1998 Oct 1;18(19):7662-73. doi: 10.1523/JNEUROSCI.18-19-07662.1998.
Nerve terminal specializations include mechanisms for maintaining a subpopulation of vesicles in a docked, fusion-ready state. We have investigated the relationship between synaptotagmin and the number of morphologically docked vesicles by an electron microscopic analysis of Drosophila synaptotagmin (syt) mutants. The overall number of synaptic vesicles in a terminal was reduced, although each active zone continued to have a cluster of vesicles in its vicinity. In addition, there was an increase in the number of large vesicles near synapses. Examining the clusters, we found that the pool of synaptic vesicles immediately adjacent to the presynaptic membrane, the pool that includes the docked population, was reduced to 24 +/- 5% (means +/- SEM) of control in the sytnull mutation. To separate contributions of overall vesicle depletion and increased spontaneous release from direct effects of synaptotagmin on morphological docking, we examined syt mutants in an altered genetic background. Recombining syt alleles onto a second chromosome bearing an as yet uncharacterized mutation resulted in the expected decrease in evoked release but suppressed the increase in spontaneous release frequency. Motor nerve terminals in this genotype contained more synaptic vesicles than control, yet the number of vesicles immediately adjacent to the presynaptic membrane near active zones was still reduced (33 +/- 4% of control). Our findings demonstrate that there is a decrease in the number of morphologically docked vesicles seen in syt mutants. The decreases in docking and evoked release are independent of the increase in spontaneous release. These results support the hypothesis that synaptotagmin stabilizes the docked state.
神经末梢特化包括将一部分囊泡维持在停靠状态(即准备好融合的状态)的机制。我们通过对果蝇突触结合蛋白(syt)突变体进行电子显微镜分析,研究了突触结合蛋白与形态学上停靠的囊泡数量之间的关系。尽管每个活性区附近仍有一群囊泡,但终末中突触囊泡的总数减少了。此外,突触附近大囊泡的数量增加。检查这些囊泡群时,我们发现紧邻突触前膜的突触囊泡池(包括停靠囊泡群体的那个池)在syt基因敲除突变体中减少到对照的24±5%(平均值±标准误)。为了区分总体囊泡耗竭和自发释放增加的影响与突触结合蛋白对形态学停靠的直接作用,我们在改变的遗传背景下检查了syt突变体。将syt等位基因重组到带有一个尚未鉴定突变的第二条染色体上,导致诱发释放预期减少,但抑制了自发释放频率的增加。这种基因型的运动神经末梢含有比对照更多的突触囊泡,然而活性区附近紧邻突触前膜的囊泡数量仍然减少(为对照的33±4%)。我们的研究结果表明,在syt突变体中可见形态学上停靠的囊泡数量减少。停靠和诱发释放的减少与自发释放的增加无关。这些结果支持了突触结合蛋白稳定停靠状态这一假说。