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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., (© 2018 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry.)

The purposes of the present study were to verify the effects of a severe thiamine deficiency episode on spatial cognitive aspects and thalamic serotonergic parameters. The animals were submitted to a severe thiamine deficiency treatment that was interrupted after the onset of the last neurological signs. The results obtained confirm previous findings about TD deficiency effects on cognitive function and, further show that this vitamin increases the thalamic serotonine metabolite, 5-hidroxyindolacetic acid (5-HIAA), level. In addition, the present data shed light on the importance of this metabolite in spatial cognitive function.