Furini Cristiane R G, Nachtigall Eduarda G, Behling Jonny A K, Assis Brasil Eduardo S, Saenger Bruna F, Narvaes Rodrigo F, de Carvalho Myskiw Jociane, Izquierdo Ivan
Memory Center, Brain Institute of Rio Grande do Sul, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Av. Ipiranga, 6690 - 2nd Floor, 90610-000 Porto Alegre, RS, Brazil; National Institute of Translational Neuroscience (INNT), National Research Council of Brazil, Brazil.
Memory Center, Brain Institute of Rio Grande do Sul, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Av. Ipiranga, 6690 - 2nd Floor, 90610-000 Porto Alegre, RS, Brazil.
Neuroscience. 2020 May 21;435:112-123. doi: 10.1016/j.neuroscience.2020.03.047. Epub 2020 Apr 6.
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.
通过一个称为巩固的过程，获取的信息被稳定到长期记忆中。然而，在巩固之后，当存储的信息被检索时，它们可能再次变得易受影响，允许修改、更新和强化，并且为了重新稳定下来，它们需要一个称为记忆重新巩固的新过程。然而，识别记忆巩固和重新巩固的分子机制尚未完全了解。此外，考虑到突触蛋白之间联系的研究是理解记忆过程的关键，我们在雄性Wistar大鼠中研究了海马体中参与物体识别记忆（ORM）巩固和重新巩固的分子机制。我们证实，在样本阶段或重新激活阶段后立即向CA1区注射AMPA受体（AMPAr）拮抗剂和L-型电压门控钙通道（L-VDCCs）阻滞剂会损害ORM的巩固和重新巩固，而这些损害可通过注射AMPAr激动剂和神经营养因子BDNF来阻断。同样，在样本阶段后3小时注射CaMKII阻滞剂会损害ORM的巩固，但对ORM的重新巩固没有影响，其作用可通过注射BDNF而不是AMPAr激动剂来阻断。因此，本研究为ORM巩固和重新巩固所涉及的分子机制提供了新证据，表明AMPAr和L-VDCCs对ORM的巩固和重新巩固是必需的，而CaMKII仅对巩固是必需的，并且在ORM的巩固和重新巩固方面，BDNF与AMPAr、L-VDCCs和CaMKII之间存在联系，以及AMPAr与L-VDCCs之间也存在联系。
