A neurobiological hypothesis of drug addiction is that it is due to a process of usurpation of the physiological mechanisms of learning and memory. Furthermore, according to the theory of reconsolidation, the long term memory, when raised, is capable of modulation can be subjected to update mechanisms. In this sense, it is possible that during the development of addiction, memory is constantly referred to and updated. This update causes several environmental cues are added to the associative memory of the original positive reinforcement. As a consequence, such cues exert a strong influence on the development of dependence, such as the occurrence of relapses commonly seen in addicts. The granule cells of the dentate gyrus are particularly important for the detection of rearrangements of order related to contextual previous experiences. Thus, these neurons are certainly recruited during the reconsolidation process and update the original memory. One form of neuronal plasticity associated with learning and memory is that neurogenesis occurs in the granular layer of the dentate gyrus. Furthermore, it is known that modulate active epigenetic process neurogenesis. One of epigenetic factors related to the resilience of these new neurons involves activation of the protein MeCP2 (methyl-CpG-binding protein 2). Interestingly, until now, there is no evidence on the role of neurogenesis in the reconsolidation of memories and update, as well as the role of MeCP2 in the process. The present study aims to study such dynamics, verifying: i. the process of neurogenesis during memory refresh, ii. and reconsolidation alter neurogenesis associated with the original memory, iii. the involvement of MeCP2 in these events. The data from this study provide important groundwork for understanding the adaptive processes involved in drug addiction.
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