Matsuzaki Masanori
Division of Biophysics, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Neurosci Res. 2007 Jan;57(1):1-9. doi: 10.1016/j.neures.2006.09.017. Epub 2006 Oct 27.
The structure of dendritic spines is highly plastic and responds to synaptic activity, including activity patterns that induce long-term potentiation (LTP) and depression (LTD). Induction of LTP causes enlargement of spine heads, while LTD causes spine head shrinkage. In addition, spine structure is well associated with synaptic weight and the extent of synaptic plasticity, such that structural changes of the spine may represent forms of memory storage. While the correlation between structural and functional plasticity appears to be simple, the underlying mechanisms of spine plasticity are intricate. Spine plasticity requires multiple molecular interactions, and is affected by the surrounding environment and by cellular metabolic state. Here, I synthesize the latest progress in this field by defining six determinants of spine plasticity, and discuss the role of each factor in memory storage.
树突棘的结构具有高度可塑性，并对突触活动做出反应，包括诱导长时程增强（LTP）和长时程抑制（LTD）的活动模式。LTP的诱导会导致棘突头部增大，而LTD则会导致棘突头部缩小。此外，棘突结构与突触权重和突触可塑性程度密切相关，因此棘突的结构变化可能代表记忆存储的形式。虽然结构可塑性和功能可塑性之间的相关性似乎很简单，但棘突可塑性的潜在机制却很复杂。棘突可塑性需要多种分子相互作用，并受周围环境和细胞代谢状态的影响。在这里，我通过定义棘突可塑性的六个决定因素来综合该领域的最新进展，并讨论每个因素在记忆存储中的作用。
