Cognition, Behavior, and Memory
Author: Matias Nicolas Schroeder | Email: maschroeder@itba.edu.ar
Matías Nicolás Schroeder 1°, Diego Moncada 1°
1° Laboratorio de Neurobiología de la Memoria, Instituto de Biología Celular y Neurociencias “Prof. E. de Robertis”, UBA-CONICET
2° Laboratorio de Bioingeniería, Departamento de Ciencias de la Vida, Instituto Tecnológico de Buenos Aires
The behavioral tagging (BT) hypothesis states that memory stabilization requires the setting of tags at experience-specific neural substrates, and the capture of newly synthesized plasticity related proteins (PRPs) at said substrates. We have previously described this mechanism in both memory consolidation and reconsolidation. Here, we study the role of the ventral tegmental area (VTA) and the D1/D5 dopaminergic receptors in the BT process underlying memory reconsolidation.
Infusion of D1/D5 dopaminergic receptors antagonist SCH23390 15 minutes before reactivation of spatial object location (SOR) memory impaired its reconsolidation. This amnesic effect could be prevented if a novel open field (OF) was explored 60 minutes before or after memory reactivation, but not 3 hours before or after. This rescuing effect was protein synthesis dependent. Furthermore, the inactivation of the VTA also prevented memory reconsolidation, effect which was once again countered by the exploration of an OF. We also saw the amnesic effect of protein synthesis inhibitor emetine (eme) could be prevented with the electrical stimulation of the VTA, provided dopaminergic receptors were functional. Finally, we analyzed molecular correlates associated with the stabilization process of a memory reactivated in the presence of SCH23390, and how the exploration of an OF affected these parameters.
Thus, our results suggest dopaminergic signaling regulated PRPs synthesis required for memory reconsolidation.