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神经细胞黏附分子在活动依赖性发育和突触可塑性中的作用

Neural cell adhesion molecules in activity-dependent development and synaptic plasticity.

作者信息

Fields R D, Itoh K

机构信息

National Institutes of Health, NICHD, Unit on Neurocytology and Physiology, Bethesda, MD 20892, USA.

出版信息

Trends Neurosci. 1996 Nov;19(11):473-80. doi: 10.1016/S0166-2236(96)30013-1.

Abstract

Cell adhesion molecules (CAMs) have a vital role in forming connections between neurons during embryonic development. Increasing evidence suggests that CAMs also participate in activity-dependent plasticity during development and synaptic plasticity in adults. Neural impulses of appropriate patterns can regulate expression of specific CAMs in mouse neurons from dorsal-root ganglia, alter cell-cell adhesion and produce structural reorganization of axon terminals in culture. Synaptic plasticity in Aplysia, learning in chick and long-term potentiation in rat hippocampus are accompanied by changes in CAM expression. Long-term potentiation can be blocked by disrupting CAM function in rat hippocampus, and learning deficits result from antibody blockade of CAMs in chicks and in transgenic mice lacking specific CAMs. Cell adhesion molecules might produce these effects by controlling several cellular processes, including cell adhesion, cytoskeletal structure and intracellular signaling.

摘要

细胞黏附分子(CAMs)在胚胎发育过程中神经元之间形成连接方面起着至关重要的作用。越来越多的证据表明,CAMs在发育过程中的活性依赖可塑性以及成体的突触可塑性中也发挥作用。适当模式的神经冲动可调节来自背根神经节的小鼠神经元中特定CAMs的表达,改变细胞间黏附并在培养物中产生轴突终末的结构重组。海兔的突触可塑性、鸡的学习以及大鼠海马体中的长时程增强都伴随着CAM表达的变化。破坏大鼠海马体中的CAM功能可阻断长时程增强,而在鸡和缺乏特定CAMs的转基因小鼠中,抗体阻断CAMs会导致学习缺陷。细胞黏附分子可能通过控制包括细胞黏附、细胞骨架结构和细胞内信号传导在内的多种细胞过程来产生这些效应。

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