Rapid plasticity of dendritic spine: hints to possible functions?
Rapid plasticity of dendritic spine: hints to possible functions?
复制标题
树突棘的快速可塑性：可能功能的暗示？
DOI：
10.1016/s0301-0082(00)00021-6
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发表时间：
2001
影响因子：
6.7
通讯作者：
M. Segal
中科院分区：
文献类型：
--
作者：
M. Segal
一个世纪以来，人们一直认为树突棘是长期记忆的稳定储存场所，但与此相反，最近一系列令人兴奋的观察使用了新的高分辨率成像方法，对培养中的活细胞进行了观察，结果显示，树突棘是一种动态结构，在数小时甚至数分钟内经历了快速的形态变化。与此同时，导致树突棘形成或塌陷的刺激的性质已经从神秘的赫布控制的可塑性产生刺激转变为更微不足道的强/弱刺激对突触的激活。脊柱可塑性的分子机制开始出现，突触前和/或突触后活动，遗传，中央或局部因素在脊柱的形成和收缩的作用目前正在分析。一个共同的机制，形成/伸长和修剪/回缩的棘，涉及细胞内钙浓度（[Ca2 +] i）的变化，正在出现。[Ca~（2+）] i与棘的变化呈钟形：突触活动的缺乏引起丝状伪足的短暂生长，但最终棘消失，[Ca~（2+）] i的适度升高引起现有棘的伸长和新棘的形成，而[Ca~（2+）] i的大量增加（如癫痫活动中所见）引起棘的快速收缩和最终塌陷。细胞核信号（如CREB）由[Ca~（2+）] i的增加激活，参与棘形成的中枢调节，而棘的收缩和伸长可能由局部[Ca~（2+）] i的变化触发。这一假说为树突棘形态学活性依赖性变化的相互矛盾的报道提供了一个简洁的解释。尽管如此，目前大多数研究都是用培养的神经元进行的，与真实的大脑中的神经元之间存在许多差异，需要对目前关于脊柱形成调控的假设进行谨慎的推断。
Contrary to a century-old belief that dendritic spines are stable storage sites of long term memory, the emerging picture from a recent flurry of exciting observations using novel high resolution imaging methods of living cells in culture is that of a dynamic structure, which undergoes fast morphological changes over periods of hours and even minutes. Concurrently, the nature of stimuli which cause formation or collapse of dendritic spines has changed from a mysterious Hebbian-governed plasticity producing stimulus to the more trivial activation of the synapse by strong/weak stimulation. The molecular mechanisms underlying spine plasticity are beginning to emerge; the role of presynaptic and/or postsynaptic activity, genetic, central or local factors in the formation and retraction of spines are currently being analyzed. A common mechanism for both, formation/elongation and pruning/retraction of spines, involving changes in intracellular calcium concentration ([Ca2+]i), is emerging. It appears that [Ca2+]iis related to changes in spines in a bell shape form: lack of synaptic activity causes transient outgrowth of filopodia but eventual elimination of spines, a moderate rise in [Ca2+]icauses elongation of existing spines and formation of new ones, while a massive increase in [Ca2+]isuch as that seen in seizure activity, causes fast shrinkage and eventual collapse of spines. Nuclear signals (e.g. CREB), activated by an increase in [Ca2+]i, are involved in the central regulation of spine formation, while spine shrinkage and elongation are probably triggered by local [Ca2+]ichanges. This hypothesis provides a parsimonious explanation for conflicting reports on activity-dependent changes in dendritic spine morphology. Still, the many differences between cultured neurons, with which most of current studies are conducted, and the neuron in the real brain, require a cautious extrapolation of current assumptions on the regulation of spine formation.
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影响因子：
56.9
作者：
RAKIC, P;BOURGEOIS, JP;GOLDMANRAKIC, PS
通讯作者：
GOLDMANRAKIC, PS
影响因子：
56.9
作者：
Shi, SH;Hayashi, Y;Malinow, R
通讯作者：
Malinow, R
DOI：
10.1073/pnas.96.23.13438
发表时间：
1999-11-09
影响因子：
11.1
作者：
Dunaevsky, A;Tashiro, A;Yuste, R
通讯作者：
Yuste, R
DOI：
10.1073/pnas.94.10.5401
发表时间：
1997-05-13
影响因子：
11.1
作者：
Comery, TA;Harris, JB;Greenough, WT
通讯作者：
Greenough, WT