Cadherin regulates dendritic spine morphogenesis
Cadherin regulates dendritic spine morphogenesis
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DOI：
10.1016/s0896-6273(02)00748-1
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发表时间：
2002-07-03
期刊：
影响因子：
16.2
通讯作者：
Takeichi, M
中科院分区：
文献类型：
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作者：
Togashi, H;Abe, K;Takeichi, M
突触重塑被认为是突触可塑性的基础机制，钙粘蛋白粘附分子被认为是这一过程的调节因子。我们研究了钙粘蛋白阻断对培养的海马神经元突触发生的影响。这种阻断导致树突棘形态的改变，如棘的丝状伪足样伸长和其头部结构的分叉，沿着伴随着突触后蛋白分布的破坏。突触前位点的突触蛋白的积累和突触囊泡回收也受到干扰，虽然这些突触反应的钙粘蛋白阻滞后变得不那么明显的突触成熟。这些研究结果表明，钙粘蛋白调节树突棘的形态发生和相关的突触功能，可能与钙粘蛋白独立的粘附机制，以维持脊柱轴突接触。
Synaptic remodeling has been postulated as a mechanism underlying synaptic plasticity, and cadherin adhesion molecules are thought to be a regulator of such a process. We examined the effects of cadherin blockage on synaptogenesis in cultured hippocampal neurons. This blockade resulted in alterations of dendritic spine morphology, such as filopodia-like elongation of the spine and bifurcation of its head structure, along with concomitant disruption of the distribution of postsynaptic proteins. The accumulation of synapsin at presynaptic sites and synaptic vesicle recycling were also perturbed, although these synaptic responses to the cadherin blockade became less evident upon the maturation of the synapses. These findings suggest that cadherin regulates dendritic spine morphogenesis and related synaptic functions, presumably cooperating with cadherin-independent adhesive mechanisms to maintain spine-axon contacts.