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突触后蛋白磷酸化与长时程增强效应

Postsynaptic protein phosphorylation and LTP.

作者信息

Soderling T R, Derkach V A

机构信息

Vollum Institute, Oregon Health Sciences University, Portland, OR 97201, USA.

出版信息

Trends Neurosci. 2000 Feb;23(2):75-80. doi: 10.1016/s0166-2236(99)01490-3.

Abstract

Prolonged changes in synaptic strength, such as those that occur in LTP and LTD, are thought to contribute to learning and memory processes. These complex phenomena occur in diverse brain structures and use multiple, temporally staged and spatially resolved mechanisms, such as changes in neurotransmitter release, modulation of transmitter receptors, alterations in synaptic structure, and regulation of gene expression and protein synthesis. In the CA1 region of the hippocampus, the combined activation of SRC family tyrosine kinases, protein kinase A, protein kinase C and, in particular, Ca2+/calmodulin-dependent protein kinase II results in phosphorylation of glutamate-receptor-gated ion channels and the enhancement of subsequent postsynaptic current. Crosstalk between these complex biochemical pathways can account for most characteristics of early-phase LTP in this region.

摘要

突触强度的长期变化,比如在长时程增强(LTP)和长时程抑制(LTD)中发生的那些变化,被认为有助于学习和记忆过程。这些复杂现象发生在不同的脑结构中,并使用多种在时间上分级且在空间上解析的机制,比如神经递质释放的变化、递质受体的调节、突触结构的改变以及基因表达和蛋白质合成的调控。在海马体的CA1区域,SRC家族酪氨酸激酶、蛋白激酶A、蛋白激酶C,尤其是Ca2+/钙调蛋白依赖性蛋白激酶II的联合激活,会导致谷氨酸受体门控离子通道的磷酸化,并增强随后的突触后电流。这些复杂生化途径之间的相互作用可以解释该区域早期LTP的大多数特征。

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