PDF(Pubmed)
Abstract：
Synapsins are highly abundant presynaptic proteins that play a crucial role in neurotransmission and plasticity via the clustering of synaptic vesicles. The synapsin III isoform is usually downregulated after development, but in hippocampal mossy fiber boutons, it persists in adulthood. Mossy fiber boutons express presynaptic forms of short- and long-term plasticity, which are thought to underlie different forms of learning. Previous research on synapsins at this synapse focused on synapsin isoforms I and II. Thus, a complete picture regarding the role of synapsins in mossy fiber plasticity is still missing. Here, we investigated presynaptic plasticity at hippocampal mossy fiber boutons by combining electrophysiological field recordings and transmission electron microscopy in a mouse model lacking all synapsin isoforms. We found decreased short-term plasticity, i.e., decreased facilitation and post-tetanic potentiation, but increased long-term potentiation in male synapsin triple knock-out (KO) mice. At the ultrastructural level, we observed more dispersed vesicles and a higher density of active zones in mossy fiber boutons from KO animals. Our results indicate that all synapsin isoforms are required for fine regulation of short- and long-term presynaptic plasticity at the mossy fiber synapse.
摘要：
突触蛋白是高度丰富的突触前蛋白，通过突触小泡的聚集在神经传递和可塑性中起关键作用。突触蛋白III亚型通常在发育后下调，但是在海马苔藓纤维束中，它在成年期仍然存在。苔藓纤维束表达短期和长期可塑性的突触前形式，被认为是不同学习形式的基础。先前对该突触的突触蛋白的研究集中在突触蛋白同工型I和II。因此，关于突触在苔藓纤维可塑性中的作用的完整图片仍然缺失。这里,我们在缺乏所有突触素同工型的小鼠模型中，通过结合电生理场记录和透射电子显微镜研究了海马苔藓纤维束的突触前可塑性。我们发现，在雄性突触素三重敲除小鼠中，短期可塑性降低-即促进和强直性后增强作用降低-但长期增强作用增加。在超微结构层面，我们观察到来自敲除动物的苔藓纤维束中更分散的囊泡和更高密度的活性区。我们的结果表明，所有突触素同工型都是苔藓纤维突触短期和长期突触前可塑性的精细调节所必需的。意义陈述突触蛋白在突触前末端聚集囊泡，并在巨大的海马苔藓纤维束形成突触前可塑性。所有突触素同工型的缺失导致短期可塑性降低但长期可塑性增加。
