Cho Kathleen Ka, Bear Mark F
The Picower Institute for Learning & Memory, Howard Hughes Medical Institute, Department of Brain & Cognitive Science, Massachusetts Institute of Technology, 77 Massachusetts Avenue, 46-3301, Cambridge, MA 02139, USA Tel.: +1 617 324 7002
Future Neurol. 2010 Jan 1;5(1):21-26. doi: 10.2217/fnl.09.62.
The modification of synapses by neural activity has been proposed to be the substrate for experience-dependent brain development, learning, and recovery of visual function after brain injury. The effectiveness or 'strength' of synaptic transmission can be persistently modified in response to defined patterns of pre- and post-synaptic activity. Well-studied examples of this type of synaptic plasticity are long-term potentiation and long-term depression. Can we exploit the current understanding of these mechanisms in order to strengthen brain connections that may have been weakened or impaired by sensory deprivation, disease or injury? Theoretically motivated research in the visual cortex has suggested ways to promote synaptic potentiation. The theoretical concept is that the type and extent of synaptic plasticity caused by patterns of activity depend critically on the recent prior history of synaptic or cellular activity. Studies in visual cortex strongly support this concept, and have suggested a mechanism for 'metaplasticity' - the plasticity of synaptic plasticity - based on activity-dependent modification of NMDA-receptor structure and function. The knowledge gained by these studies suggests ways in which recovery of function can be promoted.
神经活动对突触的修饰作用被认为是经验依赖型大脑发育、学习以及脑损伤后视觉功能恢复的基础。突触传递的有效性或“强度”能够根据突触前和突触后活动的特定模式而持续改变。这种突触可塑性的典型例子包括长期增强和长期抑制，它们都得到了充分的研究。我们能否利用目前对这些机制的理解来加强那些可能因感觉剥夺、疾病或损伤而减弱或受损的脑连接呢？视觉皮层的理论驱动研究已经提出了促进突触增强的方法。其理论概念是，由活动模式引起的突触可塑性的类型和程度关键取决于突触或细胞活动的近期历史。视觉皮层的研究有力地支持了这一概念，并基于NMDA受体结构和功能的活动依赖性修饰，提出了一种“元可塑性”（即突触可塑性的可塑性）机制。这些研究获得的知识为促进功能恢复提供了思路。
