Peineau S, Bradley C, Taghibiglou C, Doherty A, Bortolotto Z A, Wang Y T, Collingridge G L
Department of Anatomy, MRC Centre for Synaptic Plasticity, School of Medical sciences, University Walk, Bristol, UK.
Br J Pharmacol. 2008 Mar;153 Suppl 1(Suppl 1):S428-37. doi: 10.1038/bjp.2008.2.
Glycogen synthase kinase-3 (GSK-3), an important component of the glycogen metabolism pathway, is highly expressed in the CNS. It has been implicated in major neurological disorders including Alzheimer's disease, schizophrenia and bipolar disorders. Despite its central role in these conditions it was not known until recently whether GSK-3 has neuronal-specific functions under normal conditions. However recent work has shown that GSK-3 is involved in the regulation of, and cross-talk between, two major forms of synaptic plasticity, N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) and NMDAR-dependent long-term depression (LTD). The present article summarizes this recent work and discusses its potential relevance to the treatment of neurological disorders.
糖原合酶激酶-3（GSK-3）是糖原代谢途径的重要组成部分，在中枢神经系统中高度表达。它与包括阿尔茨海默病、精神分裂症和双相情感障碍在内的主要神经疾病有关。尽管它在这些疾病中起着核心作用，但直到最近人们还不清楚GSK-3在正常情况下是否具有神经元特异性功能。然而，最近的研究表明，GSK-3参与了两种主要形式的突触可塑性——N-甲基-D-天冬氨酸受体（NMDAR）依赖性长时程增强（LTP）和NMDAR依赖性长时程抑制（LTD）的调节以及它们之间的相互作用。本文总结了这项最新研究，并讨论了其与神经疾病治疗的潜在相关性。
