Segal I, Korkotian I, Murphy D D
Dept of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel.
Trends Neurosci. 2000 Feb;23(2):53-7. doi: 10.1016/s0166-2236(99)01499-x.
The recent advent of novel high-resolution imaging methods has created a flurry of exciting observations that address a century-old question: what are biological signals that regulate formation and elimination of dendritic spines? Contrary to the traditional belief that the spine is a stable storage site of long-term neuronal memory, the emerging picture is of a dynamic structure that can undergo fast morphological variations. Recent conflicting reports on the regulation of spine morphology lead to the proposal of a unifying hypothesis for a common mechanism involving changes in postsynaptic intracellular Ca2+ concentration, [Ca2+]i: a moderate rise in [Ca2+]i causes elongation of dendritic spines, while a very large increase in [Ca2+]i causes fast shrinkage and eventual collapse of spines. This hypothesis provides a parsimonious explanation for conflicting reports on activity-dependent changes in dendritic spine morphology, and might link these changes to functional plasticity in central neurons.
最近，新型高分辨率成像方法的出现带来了一系列令人兴奋的观察结果，这些结果解决了一个存在了百年的问题：调节树突棘形成和消除的生物信号是什么？与传统观念中树突棘是长期神经元记忆的稳定存储位点相反，新出现的情况表明它是一种动态结构，能够经历快速的形态变化。最近关于树突棘形态调节的相互矛盾的报道，促使人们提出了一个统一的假说，即涉及突触后细胞内Ca2+浓度（[Ca2+]i）变化的共同机制：[Ca2+]i适度升高会导致树突棘伸长，而[Ca2+]i大幅增加则会导致树突棘快速收缩并最终塌陷。这一假说为关于树突棘形态依赖活动变化的相互矛盾的报道提供了一个简洁的解释，并可能将这些变化与中枢神经元的功能可塑性联系起来。
