Owe Simen G, Jensen Vidar, Evergren Emma, Ruiz Arnaud, Shupliakov Oleg, Kullmann Dimitri M, Storm-Mathisen Jon, Walaas S Ivar, Hvalby Øivind, Bergersen Linda H
Department of Anatomy, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Cereb Cortex. 2009 Mar;19(3):511-23. doi: 10.1093/cercor/bhn101. Epub 2008 Jun 11.
The synapsin proteins have different roles in excitatory and inhibitory synaptic terminals. We demonstrate a differential role between types of excitatory terminals. Structural and functional aspects of the hippocampal mossy fiber (MF) synapses were studied in wild-type (WT) mice and in synapsin double-knockout mice (DKO). A severe reduction in the number of synaptic vesicles situated more than 100 nm away from the presynaptic membrane active zone was found in the synapsin DKO animals. The ultrastructural level gave concomitant reduction in F-actin immunoreactivity observed at the periactive endocytic zone of the MF terminals. Frequency facilitation was normal in synapsin DKO mice at low firing rates (approximately 0.1 Hz) but was impaired at firing rates within the physiological range (approximately 2 Hz). Synapses made by associational/commissural fibers showed comparatively small frequency facilitation at the same frequencies. Synapsin-dependent facilitation in MF synapses of WT mice was attenuated by blocking F-actin polymerization with cytochalasin B in hippocampal slices. Synapsin III, selectively seen in MF synapses, is enriched specifically in the area adjacent to the synaptic cleft. This may underlie the ability of synapsin III to promote synaptic depression, contributing to the reduced frequency facilitation observed in the absence of synapsins I and II.
突触素蛋白在兴奋性和抑制性突触终末具有不同作用。我们证明了不同类型兴奋性终末之间存在差异作用。在野生型(WT)小鼠和突触素双敲除小鼠(DKO)中研究了海马苔藓纤维(MF)突触的结构和功能方面。在突触素DKO动物中,发现距离突触前膜活性区超过100 nm的突触小泡数量严重减少。超微结构水平上,MF终末活性内吞区的F-肌动蛋白免疫反应性也随之降低。在低发放频率(约0.1 Hz)时,突触素DKO小鼠的频率易化正常,但在生理范围内的发放频率(约2 Hz)时受损。联合/连合纤维形成的突触在相同频率下表现出相对较小的频率易化。在海马切片中用细胞松弛素B阻断F-肌动蛋白聚合可减弱WT小鼠MF突触中依赖突触素的易化。在MF突触中特异性可见的突触素III,在突触间隙相邻区域特别富集。这可能是突触素III促进突触抑制的能力的基础,导致在缺乏突触素I和II时观察到的频率易化降低。