期刊
NEURON
卷 53, 期 5, 页码 703-717出版社
CELL PRESS
DOI: 10.1016/j.neuron.2007.01.029
关键词
-
资金
- Medical Research Council [G9532377] Funding Source: Medline
- MRC [G9532377] Funding Source: UKRI
- Medical Research Council [G9532377] Funding Source: researchfish
Glycogen synthase kinase-3 (GSK3) has been implicated in major neurological disorders, but its role in normal neuronal function is largely unknown. Here we show that GSK3 beta mediates an interaction between two major forms of synaptic plasticity in the brain, N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) and NMDA receptor-dependent long-term depression (LTD). In rat hippocampal slices, GSK3 beta inhibitors block the induction of LTD. Furthermore, the activity of GSK3 beta is enhanced during LTD via activation of PP1. Conversely, following the induction of LTP, there is inhibition of GSK3 beta activity. This regulation of GSK3 beta during LTP involves activation of NMDA receptors and the PI3K-Akt pathway and disrupts the ability of synapses to undergo LTD for up to 1 hr. We conclude that the regulation of GSK3 beta activity provides a powerful mechanism to preserve information encoded during LTP from erasure by subsequent LTD, perhaps thereby permitting the initial consolidation of learnt information.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据