Cognition, Behavior, and Memory
Author: MATIAS NICOLAS SCHROEDER | email: matias.nicolas.sch@gmail.com
Matias Nicolas Schroeder 1°, Diego Moncada 1°
1° Facultad de Medicina, Instituto de Biología Celular y Neurociencia Prof. E. De Robertis (IBCN), UBA-CONICET, Buenos Aires, Argentina
2° Instituto Tecnológico de Buenos Aires, Buenos Aires, Argentina
The behavioral tagging (BT) hypothesis postulates that memory stabilization relies on the setting of experience-specific tags at appropriate neural substrates, and the capture of newly synthesized plasticity related proteins (PRPs) at said substrates. We have previously shown this mechanism underlies both memory consolidation and reconsolidation. Here, we study the role of the locus coeruleus (LC) and the ?-adrenergic in the BT process underlying memory reconsolidation. Infusion of ?-adrenergic receptors antagonist propranolol 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 after. This rescuing effect was protein synthesis dependent. Furthermore, the inactivation of the LC also prevented memory reconsolidation, effect which was once again countered by the exploration of a OF. We also saw the amnesic effect of protein synthesis inhibitor emetine (eme) could be prevented with the electrical stimulation of the LC, provided ?-adrenergic receptors were functional. Finally, we analyzed the expression of proteins associated to memory stabilization after memory was reactivated in the presence of propranolol, and how the exploration of an OF affected this expression. Taken together, these results suggest noradrenergic signaling regulated PRPs synthesis required for memory reconsolidation.