Department of Cell and Integrative Physiology, The University of Texas Health San Antonio, 8403, Floyd Curl Drive, San Antonio, TX 78229, USA.
Department of Basic and Clinical Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, UK.
J Neurochem. 2018 Oct;147(1):12-23. doi: 10.1111/jnc.14454. Epub 2018 Jun 27.
In this review, we discuss the poorly explored role of calcium/calmodulin-dependent protein kinase II (CaMKII) in memory maintenance, and its influence on memory destabilization. After a brief review on CaMKII and memory destabilization, we present critical pieces of evidence suggesting that CaMKII activity increases retrieval-induced memory destabilization. We then proceed to propose two potential molecular pathways to explain the association between CaMKII activation and increased memory destabilization. This review will pinpoint gaps in our knowledge and discuss some 'controversial' observations, establishing the basis for new experiments on the role of CaMKII in memory reconsolidation. The role of CaMKII in memory destabilization is of great clinical relevance. Still, because of the lack of scientific literature on the subject, more basic science research is necessary to pursue this pathway as a clinical tool.
在这篇综述中,我们讨论了钙/钙调蛋白依赖性蛋白激酶 II(CaMKII)在记忆维持中的作用尚未被充分探索,以及它对记忆不稳定的影响。在简要回顾 CaMKII 和记忆不稳定之后,我们提出了一些关键证据,表明 CaMKII 活性增加了检索诱导的记忆不稳定。然后,我们提出了两种潜在的分子途径来解释 CaMKII 激活与增加的记忆不稳定之间的关联。这篇综述将指出我们知识中的空白,并讨论一些“有争议”的观察结果,为 CaMKII 在记忆再巩固中的作用的新实验奠定基础。CaMKII 在记忆不稳定中的作用具有重要的临床意义。然而,由于缺乏关于该主题的科学文献,因此需要更多的基础科学研究来将该途径作为一种临床工具进行探索。