Tong Rudi, Chater Thomas Edward, Emptage Nigel John, Goda Yukiko
University of Oxford, Department of Pharmacology, Mansfield Rd, Oxford OX1 3QT, UK.
RIKEN Center for Brain Science, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
Cell Rep. 2021 Jan 26;34(4):108693. doi: 10.1016/j.celrep.2021.108693.
Dendrites are crucial for integrating incoming synaptic information. Individual dendritic branches are thought to constitute a signal processing unit, yet how neighboring synapses shape the boundaries of functional dendritic units is not well understood. Here, we address the cellular basis underlying the organization of the strengths of neighboring Schaffer collateral-CA1 synapses by optical quantal analysis and spine size measurements. Inducing potentiation at clusters of spines produces NMDA-receptor-dependent heterosynaptic plasticity. The direction of postsynaptic strength change shows distance dependency to the stimulated synapses where proximal synapses predominantly depress, whereas distal synapses potentiate; potentiation and depression are regulated by CaMKII and calcineurin, respectively. In contrast, heterosynaptic presynaptic plasticity is confined to weakening of presynaptic strength of nearby synapses, which requires CaMKII and the retrograde messenger nitric oxide. Our findings highlight the parallel engagement of multiple signaling pathways, each with characteristic spatial dynamics in shaping the local pattern of synaptic strengths.
树突对于整合传入的突触信息至关重要。单个树突分支被认为构成一个信号处理单元，然而相邻突触如何塑造功能性树突单元的边界尚不清楚。在这里，我们通过光学量子分析和棘突大小测量来探讨相邻的谢弗侧支 - CA1 突触强度组织的细胞基础。在棘突簇处诱导增强会产生 NMDA 受体依赖性异突触可塑性。突触后强度变化的方向显示出与受刺激突触的距离依赖性，其中近端突触主要抑制，而远端突触增强；增强和抑制分别由 CaMKII 和钙调神经磷酸酶调节。相比之下，异突触前突触可塑性仅限于附近突触的突触前强度减弱，这需要 CaMKII 和逆行信使一氧化氮。我们的研究结果突出了多种信号通路的并行参与，每条通路在塑造突触强度的局部模式方面都具有独特的空间动态。
