期刊
FRONTIERS IN MOLECULAR NEUROSCIENCE
卷 5, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2012.00013
关键词
GSK-3 (glycogen synthase kinase-3); caspase 3; Akt (PKB; protein kinase B); synaptic plasticity; LTP (long-term potentiation); LTD (long-term depression); AMPAR (AMPA receptor); NMDAR (NMDA receptor)
资金
- MRC
- BBSRC
- Wellcome Trust
- CIHR
- Korean Ministry of Science and Technology
- WCU program through the KOSEF - MEST [R31-10089]
- Creative Research Initiatives Program of the Korean Ministry of Science and Technology
- Inserm
- Universite Paris Diderot
- PremUP
- Fondation Roger de Spoelberch
- Fondation Grace de Monaco
- Leducq Foundation
- Biotechnology and Biological Sciences Research Council [BB/G003963/1] Funding Source: researchfish
- Medical Research Council [MC_G1000734, G0601841B, G0601813] Funding Source: researchfish
- BBSRC [BB/G003963/1] Funding Source: UKRI
- MRC [MC_G1000734, G0601813] Funding Source: UKRI
Glycogen synthase kinase-3 (GSK-3) has many cellular functions. Recent evidence suggests that it plays a key role in certain types of synaptic plasticity, in particular a form of long-term depression (LTD) that is induced by the synaptic activation of N-methyl-D-aspartate receptors (NMDARs). In the present article we summarize what is currently known concerning the roles of GSK-3 in synaptic plasticity at both glutamatergic and GABAergic synapses. We summarize its role in cognition and speculate on how alterations in the synaptic functioning of GSK-3 may be a major factor in certain neurodegenerative disorders.
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