Brodin L, Löw P, Gad H, Gustafsson J, Pieribone V A, Shupliakov O
Department of Neuroscience, Nobel Institute for Neurophysiology, Karolinska Institutet, Stockholm, Sweden.
Eur J Neurosci. 1997 Dec;9(12):2503-11. doi: 10.1111/j.1460-9568.1997.tb01679.x.
Chemical synapses convey impulses at high frequency by exocytosis of synaptic vesicles. To avoid failure of synaptic transmission, rapid replenishment of synaptic vesicles must occur. Recent molecular perturbation studies have confirmed that the recycling of synaptic vesicles involves clathrin-mediated endocytosis. The rate of exocytosis would thus be limited by the capacity of the synaptic clathrin machinery unless vesicles could be drawn from existing pools. The mobilization of vesicles from the pool clustered at the release sites appears to provide a mechanism by which the rate of exocytosis can intermittently exceed the rate of recycling. Perturbation of synapsins causes disruption of vesicle clusters and impairment of synaptic transmission at high but not at low frequencies. Both clathrin-mediated recycling and mobilization of vesicles from the reserve pool are thus important in the replenishment of synaptic vesicles. The efficacy of each mechanism appears to differ between synapses which operate with different patterns of activity.
化学突触通过突触小泡的胞吐作用高频传递冲动。为避免突触传递失败，必须快速补充突触小泡。最近的分子扰动研究证实，突触小泡的循环利用涉及网格蛋白介导的内吞作用。因此，除非小泡能从现有储备池中获取，否则胞吐速率将受突触网格蛋白机制能力的限制。从聚集在释放位点的储备池中动员小泡似乎提供了一种机制，通过该机制胞吐速率可以间歇性地超过循环利用速率。突触结合蛋白的扰动会导致小泡簇的破坏以及高频而非低频时突触传递的受损。因此，网格蛋白介导的循环利用和从储备池中动员小泡在突触小泡的补充中都很重要。每种机制的功效在以不同活动模式运作的突触之间似乎有所不同。
