Doherty P, Fazeli M S, Walsh F S
Department of Experimental Pathology, UMDS, Guy's Hospital, London, United Kingdom.
J Neurobiol. 1995 Mar;26(3):437-46. doi: 10.1002/neu.480260315.
Highly stereotyped patterns of neuronal connections are laid down during the development of the nervous system via a range of activity independent and activity dependent mechanisms. Whereas the coarse hard-wiring of the nervous system appears to rely on molecular recognition events between the neuron, its pathway, and its target, the establishment of precisely patterned functional circuits is thought to be driven by neuronal activity. In this review we discuss the role that the neuronal cell adhesion molecule (NCAM) plays in morphological plasticity. Recent studies on NCAM and its probable species homologue in Aplysia (apCAM) suggests that an individual CAM can function to both promote synaptic plasticity and maintain the structure of the synapse. In the adult brain, changes between stability and plasticity are likely to underlie dynamic morphological changes in synaptic structures associated with learning and memory. In this review we use NCAM as an example to illustrate mechanisms that can change the function of an individual CAM from a molecule that promotes plasticity to one that does not. We also discuss evidence that NCAM promotes plasticity by activating a conventional signal transduction cascade, rather than by modulating adhesion per se. Finally, we consider the evidence that supports a role for NCAM in learning and memory.
在神经系统发育过程中，高度刻板的神经元连接模式是通过一系列与活动无关和与活动有关的机制建立起来的。虽然神经系统的粗略硬连线似乎依赖于神经元与其通路及靶标之间的分子识别事件，但精确模式化功能回路的建立被认为是由神经元活动驱动的。在这篇综述中，我们讨论神经元细胞黏附分子（NCAM）在形态可塑性中所起的作用。最近对NCAM及其在海兔中可能的物种同源物（apCAM）的研究表明，单个细胞黏附分子既能促进突触可塑性，又能维持突触结构。在成体大脑中，稳定性和可塑性之间的变化可能是与学习和记忆相关的突触结构动态形态变化的基础。在这篇综述中，我们以NCAM为例来说明可以将单个细胞黏附分子的功能从促进可塑性的分子转变为不促进可塑性的分子的机制。我们还讨论了NCAM通过激活传统信号转导级联反应而非通过调节黏附本身来促进可塑性的证据。最后，我们考虑支持NCAM在学习和记忆中发挥作用的证据。
