Tompa P, Friedrich P
Institute of Enzymology, Biological Research Center, Hungarian Academy of Sciences, Budapest.
Trends Neurosci. 1998 Mar;21(3):97-102. doi: 10.1016/s0166-2236(97)01176-4.
Synaptic plasticity might be one of the elementary processes that underlies higher brain functions, such as learning and memory. Intriguingly, the capacity of a synapse for plastic changes itself displays marked variation or plasticity. This higher-order plasticity, or metaplasticity, appears to depend on the same macromolecules as plasticity, most notably the NMDA receptor and Ca2+/calmodulin kinase II; yet we do not understand metaplasticity in molecular terms. Metaplasticity has a feedback-inhibition character that confers stability to synaptic patterns, whereas in plasticity, the molecular events implicated tend to have an opposite effect. As a resolution to this difference, we suggest that metaplasticity be considered in a biophysical context. It has been shown that autophosphorylation of Ca2+/calmodulin kinase II in postsynaptic densities generates changes in the local electrostatic potential sufficient to affect the direction of synaptic plasticity. We propose that this finding could help explain both the puzzling abundance of Ca2+/calmodulin kinase II in the postsynaptic density and the metaplasticity of synaptic transmission.
突触可塑性可能是构成诸如学习和记忆等高级脑功能基础的基本过程之一。有趣的是，突触自身进行可塑性变化的能力表现出显著的差异或可塑性。这种高阶可塑性，即元可塑性，似乎依赖于与可塑性相同的大分子，最显著的是NMDA受体和Ca2+/钙调蛋白激酶II；然而，我们并不从分子层面理解元可塑性。元可塑性具有反馈抑制特性，赋予突触模式稳定性，而在可塑性方面，涉及的分子事件往往具有相反的作用。作为对这种差异的一种解释，我们建议在生物物理背景下考虑元可塑性。已经表明，突触后致密物中Ca2+/钙调蛋白激酶II的自磷酸化会产生足以影响突触可塑性方向的局部静电势变化。我们提出这一发现有助于解释突触后致密物中令人困惑的大量Ca2+/钙调蛋白激酶II以及突触传递的元可塑性。
