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STRUCTURAL PLASTICITY AND MEMORY

机译:结构可塑性和记忆

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Much evidence indicates that, after learning, memories are created by alterations in glutamate-dependent excitatory synaptic transmission. These modifications are then actively stabilized, over hours or days, by structural changes at postsynaptic sites on dendritic spines. The mechanisms of this structural plasticity are poorly understood, but recent findings are beginning to provide clues. The changes in synaptic transmission are initiated by elevations in intracelluiar calcium and consequent activation of second messenger signalling pathways in the postsynaptic neuron. These pathways involve intracelluiar kinases and GTPases, downstream from glutamate receptors, that regulate and coordinate both cytoskeletal and adhesion remodelling, leading to new synaptic connections. Rapid changes in cytoskeletal and adhesion molecules after learning contribute to short-term plasticity and memory, whereas later changes, which depend on de novo protein synthesis as well as the early modifications, seem to be required for the persistence of long-term memory.
机译:许多证据表明,学习后,记忆是通过改变谷氨酸依赖性兴奋性突触传递而产生的。然后,这些修饰通过树突棘上突触后位点的结构变化在数小时或数天内被主动稳定化。人们对这种结构可塑性的机制了解甚少,但是最近的发现开始提供线索。突触传递的变化是由细胞内钙的升高和突触后神经元中第二信使信号通路的激活引起的。这些途径涉及谷氨酸受体下游的细胞内激酶和GTP酶,它们调节和协调细胞骨架和粘附重塑,导致新的突触连接。学习后细胞骨架和粘附分子的快速变化有助于短期可塑性和记忆,而依赖于从头蛋白质合成以及早期修饰的后期变化似乎是持久记忆的持久性所必需的。

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