α钙调蛋白激酶II自身磷酸化：通往记忆的快速通道。
alphaCaMKII autophosphorylation: a fast track to memory.
作者信息
Irvine Elaine E, von Hertzen Laura S J, Plattner Florian, Giese Karl Peter
机构信息
Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.
出版信息
Trends Neurosci. 2006 Aug;29(8):459-65. doi: 10.1016/j.tins.2006.06.009. Epub 2006 Jun 27.
Alpha Ca(2+)/calmodulin-dependent kinase II (alphaCaMKII), the major synaptic protein in the forebrain, can switch into a state of autonomous activity upon autophosphorylation. It has been proposed that alphaCaMKII autophosphorylation mediates long-term memory (LTM) storage. However, recent evidence shows that synaptic stimulation and behavioural training only transiently increase the autonomous alphaCaMKII activity, implicating alphaCaMKII autophosphorylation in LTM formation rather than storage. Consistent with this, mutant mice deficient in alphaCaMKII autophosphorylation can store LTM after a massed training protocol, but cannot form LTM after a single trial. Here, we review evidence that the role of alphaCaMKII autophosphorylation is in fact to enable LTM formation after a single training trial, possibly by regulating LTM consolidation-specific transcription.
α钙调蛋白依赖性蛋白激酶II（αCaMKII）是前脑主要的突触蛋白，自磷酸化后可转变为自主活动状态。有人提出，αCaMKII自磷酸化介导长期记忆（LTM）的存储。然而，最近的证据表明，突触刺激和行为训练只会短暂增加αCaMKII的自主活性，这表明αCaMKII自磷酸化与LTM形成有关，而非存储。与此一致的是，缺乏αCaMKII自磷酸化的突变小鼠在集中训练后可以存储LTM，但单次试验后无法形成LTM。在此，我们综述了相关证据，即αCaMKII自磷酸化的作用实际上是在单次训练后使LTM形成，可能是通过调节LTM巩固特异性转录来实现的。
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