Banca de QUALIFICAÇÃO: DIANA ALINE NOGA MORAIS FERREIRA

Uma banca de QUALIFICAÇÃO de DOUTORADO foi cadastrada pelo programa.
DISCENTE : DIANA ALINE NOGA MORAIS FERREIRA
DATA : 25/10/2017
HORA: 14:30
LOCAL: Sala de Aula do PPg em Psicobiologia
TÍTULO:

On the Role of mTOR signaling in Reconsolidation of Extinction Memory

PALAVRAS-CHAVES:

Reconsolidation; Extinction; BDNF; CA1; mTORC1; Rapamycin.

PÁGINAS: 28
GRANDE ÁREA: Ciências Humanas
ÁREA: Psicologia
RESUMO:

Reactivation of a memory may induce two apparently opposite phenomenons, extinction and reconsolidation. Extinction involves the reduction of a previously learned aversive response, which seems to result on the formation of a new and opposite memory trace. In the other hand, reconsolidation seems to involve a modification of a preformed memory trace in order to strengthen or update this trace. Several studies discuss the opposition between extinction and reconsolidation, putting the first as a boundary condition for the second. However, little attention is given to a possible interaction between these two processes. Previous studies from our group showed that an extinction memory can be reconsolidated and this process is dependent on BDNF via its TrKB receptor. TrKB activates three intracellular cascades (Shc, PLC and PI3K). Considering the prominent role of PI3K/AkT/mTOR pathway in plasticity, this study aims to investigate the possible role of hippocampal mTOR during the reconsolidation of extinction memory. For that purpose, we will perform four experiments with Wistar rats. The first experiment aims to determine if inhibition of mTORC1 by infusion of rapamycin in CA1 impairs reconsolidation. The second experiment aims to investigate if reconsolidation of extinction memory is accompanied by increases in expression and/or activation of mTOR, its main substrates and GluA1. The third aims to determine the role of mTOR in a possible increase in GluA1 expression and/or phosphorylation. Lastly, the fourth experiment aims to verify that BDNF is acting upstream to mTOR in this cascade. Our preliminary results showed that rapamycin administration immediately after reactivation causes the return of the previously learned aversive response. This suggests that inhibition of mTORC1 impairs reconsolidation of extinction memory.

MEMBROS DA BANCA:
Interno - 1644341 - ANA CAROLINA LUCHIARI
Interno - 1645202 - ELAINE CRISTINA GAVIOLI
Presidente - 1996111 - MARTIN PABLO CAMMAROTA