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A pivotal role of GSK-3 in synaptic plasticity

期刊

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

  1. MRC
  2. BBSRC
  3. Wellcome Trust
  4. CIHR
  5. Korean Ministry of Science and Technology
  6. WCU program through the KOSEF - MEST [R31-10089]
  7. Creative Research Initiatives Program of the Korean Ministry of Science and Technology
  8. Inserm
  9. Universite Paris Diderot
  10. PremUP
  11. Fondation Roger de Spoelberch
  12. Fondation Grace de Monaco
  13. Leducq Foundation
  14. Biotechnology and Biological Sciences Research Council [BB/G003963/1] Funding Source: researchfish
  15. Medical Research Council [MC_G1000734, G0601841B, G0601813] Funding Source: researchfish
  16. BBSRC [BB/G003963/1] Funding Source: UKRI
  17. MRC [MC_G1000734, G0601813] Funding Source: UKRI

向作者/读者索取更多资源

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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