Promoting neurological recovery of function via metaplasticity
Promoting neurological recovery of function via metaplasticity
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DOI：
10.2217/fnl.09.62
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发表时间：
2010-01-01
期刊：
影响因子：
1.3
通讯作者：
Bear, Mark F.
中科院分区：
文献类型：
--
作者：
Cho, Kathleen K. A.;Bear, Mark F.
神经活动对突触的修饰被认为是脑损伤后经验依赖性脑发育、学习和视觉功能恢复的基础。突触传递的有效性或“强度”可以根据突触前和突触后活动的定义模式而持续改变。这种类型的突触可塑性研究的例子是长时程增强和长时程抑制。我们能否利用目前对这些机制的理解来加强可能因感觉剥夺、疾病或伤害而减弱或受损的大脑连接？视觉皮层的理论研究已经提出了促进突触增强的方法。理论上的概念是，由活动模式引起的突触可塑性的类型和程度严重依赖于突触或细胞活动的近期历史。视觉皮层的研究强烈支持这一概念，并提出了一种基于NMDA受体结构和功能的活性依赖性修饰的“元可塑性”机制-突触可塑性的可塑性。通过这些研究获得的知识表明了可以促进功能恢复的方法。
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 preand 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.