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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Molecular Mechanisms in Hippocampus Involved on Object Recognition Memory Consolidation and Reconsolidation
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Molecular Mechanisms in Hippocampus Involved on Object Recognition Memory Consolidation and Reconsolidation

机译:海马中的分子机制涉及物体识别记忆合并和重新垄断的

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Acquired information is stabilized into long-term memory through a process known as consolidation. Though, after consolidation, when stored information is retrieved they can be again susceptible, allowing modification, updating and strengthening and to be re-stabilized they need a new process referred to as memory reconsolidation. However, the molecular mechanisms of recognition memory consolidation and reconsolidation are not fully understood. Also, considering that the study of the link between synaptic proteins is key to understanding of memory processes, we investigated, in male Wistar rats, molecular mechanisms in the hippocampus involved on object recognition memory (ORM) consolidation and reconsolidation. We verified that the blockade of AMPA receptors (AMPAr) and L-VDCCs calcium channels impaired ORM consolidation and reconsolidation when administered into CA1 immediately after sample phase or reactivation phase and that these impairments were blocked by the administration of AMPAr agonist and of neurotrophin BDNF. Also, the blockade of CaMKII impaired ORM consolidation when administered 3 h after sample phase but had no effect on ORM reconsolidation and its effect was blocked by the administration of BDNF, but not of AMPAr agonist. So, this study provides new evidence of the molecular mechanisms involved on the consolidation and reconsolidation of ORM, demonstrating that AMPAr and L-VDCCs are necessary for the consolidation and reconsolidation of ORM while CaMKII is necessary only for the consolidation and also that there is a link between BDNF and AMPAr, L-VDCCs and CaMKII as well as a link between AMPAr and L-VDCCs on ORM consolidation and reconsolidation. (C) 2020 Published by Elsevier Ltd on behalf of IBRO.
机译:获取的信息通过称为合并的过程稳定为长期记忆。虽然,在整合之后,当检索存储的信息时,它们可以再次易感,允许修改,更新和加强并重新稳定,他们需要一个新的过程称为内存再谐波。然而,识别记忆合并和重新垄断的分子机制不完全理解。此外,考虑到突触蛋白之间的联系的研究是了解记忆过程的关键,我们在雄性Wistar大鼠中研究了对象识别记忆(ORM)固结和重新垄断的海马中的分子机制。我们核实随着在样品相或再激活阶段的样品或再激活阶段施用的情况下施用进入CA1时,AMPA受体(AMPAR)和L-VDCCS钙通道的阻断障碍和再共聚势率受损,并且通过施用AMPAR激动剂和神经营养蛋白BDNF阻断这些损伤。此外,当样品相后3小时施用3小时但没有对ORM重新溶解的影响,并且其作用被BDNF施用,但不含AMPAR激动剂,而不是AMPAR激动剂的影响。因此,本研究提供了新的证据证明涉及orm的整合和重新垄断的分子机制,证明AMPAR和L-VDCC是营收综合和重新垄断的副本,而CAMKII仅用于整合,也有一个BDNF和AMPAR,L-VDCC和Camkii之间的链接以及AMPAR和L-VDCC之间的链接,ORM整合和重新定位。 (c)2020年由elsevier有限公司发布代表银布。

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