Structural plasticity can produce metaplasticity.
Structural plasticity can produce metaplasticity.
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DOI：
10.1371/journal.pone.0008062
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发表时间：
2009-11-30
期刊：
影响因子：
3.7
通讯作者：
Shouval HZ
中科院分区：
文献类型：
--
作者：
Kalantzis G;Shouval HZ
突触可塑性是学习、记忆和发育的基础。突触可塑性的性质可以作为先前的可塑性和先前的突触激活的函数而改变，这种现象称为超可塑性。突触可塑性不仅改变了神经元之间的功能连接，而且在某些情况下会产生突触棘的结构变化;这种变化被认为是这种观察到的可塑性的基础。在这里，我们研究在何种程度上的结构可塑性的棘可以是一个原因的超塑性。本研究的动机是观察到，在脊柱的结构变化可能会影响在脊柱钙动力学。由于钙动力学决定了突触可塑性的标志和大小，因此结构可塑性可能会改变突触可塑性的性质。在这项研究中，我们解决的问题，脊柱几何形状和N-甲基-D-天冬氨酸（NMDA）受体电导的改变可能会影响可塑性。基于一个简化的模型，结合钙依赖的可塑性规则的脊柱，我们证明了后的诱导阶段的可塑性移位的长时程增强（LTP）或长时程抑制（LTD）阈值发生。这诱导了进一步LTP诱导的不应期，并促进了实验观察到的去增强作用。这类似于神经元可塑性规则，但对单个突触来说是特定的。在第二阶段中，NMDA响应的改变可以使突触达到使得进一步突触权重改变是可行的状态。我们发现，如果NMDA反应的增强是成正比的突触后密度（PSD）的可塑性曲线最有可能返回到初始状态。使用模拟突触棘中的钙动力学，再加上生物药理学动机的钙依赖性可塑性规则，我们发现在什么条件下结构可塑性可以形成突触特异性超可塑性的基础。
Synaptic plasticity underlies many aspect of learning memory and development. The properties of synaptic plasticity can change as a function of previous plasticity and previous activation of synapses, a phenomenon called metaplasticity. Synaptic plasticity not only changes the functional connectivity between neurons but in some cases produces a structural change in synaptic spines; a change thought to form a basis for this observed plasticity. Here we examine to what extent structural plasticity of spines can be a cause for metaplasticity. This study is motivated by the observation that structural changes in spines are likely to affect the calcium dynamics in spines. Since calcium dynamics determine the sign and magnitude of synaptic plasticity, it is likely that structural plasticity will alter the properties of synaptic plasticity. In this study we address the question how spine geometry and alterations of N-methyl-D-aspartic acid (NMDA) receptors conductance may affect plasticity. Based on a simplified model of the spine in combination with a calcium-dependent plasticity rule, we demonstrated that after the induction phase of plasticity a shift of the long term potentiation (LTP) or long term depression (LTD) threshold takes place. This induces a refractory period for further LTP induction and promotes depotentiation as observed experimentally. That resembles the BCM metaplasticity rule but specific for the individual synapse. In the second phase, alteration of the NMDA response may bring the synapse to a state such that further synaptic weight alterations are feasible. We show that if the enhancement of the NMDA response is proportional to the area of the post synaptic density (PSD) the plasticity curves most likely return to the initial state. Using simulations of calcium dynamics in synaptic spines, coupled with a biophysically motivated calcium-dependent plasticity rule, we find under what conditions structural plasticity can form the basis of synapse specific metaplasticity.
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影响因子：
4.8
作者：
Mainen, ZF;Maletic-Savatic, M;Svoboda, K
通讯作者：
Svoboda, K
DOI：
10.1073/pnas.201404598
发表时间：
2001-10-23
影响因子：
11.1
作者：
Castellani, GC;Quinlan, EM;Shouval, HZ
通讯作者：
Shouval, HZ
影响因子：
16.2
作者：
Cummings, JA;Mulkey, RM;Malenka, RC
通讯作者：
Malenka, RC
DOI：
10.1007/bf01261506
发表时间：
1977-01-01
期刊：
JOURNAL OF NEUROCYTOLOGY
影响因子：
--
作者：
FIFKOVA, E;VANHARREVELD, A
通讯作者：
VANHARREVELD, A
影响因子：
64.8
作者：
Engert, F;Bonhoeffer, T
通讯作者：
Bonhoeffer, T