The behavioral tagging (BT) hypothesis proposes that lasting memories require the synthesis of plasticity-related proteins (PRPs) and the setting of a learning tag. The latter will capture the PRPs to stabilize the memory trace. We have previously shown that memory reconsolidation also fits this model. Here, we show that the dopaminergic and noradrenergic systems specifically regulate the synthesis of PRPs in the BT process during memory reconsolidation.
Using a spatial object recognition task (SOR) in rats, we show that antagonizing the hippocampal D1/D5-dopaminergic, or the β-adrenergic receptors, during memory reactivation impaired its reconsolidation. However, this requirement was overcome by the exploration of a novel open field (NOF) within a critical time window around the reactivation session. This phenomenon was dependent on PRPs synthesis triggered by the novel experience. Moreover, behavioral novelty could be replaced by the electric stimulation of the VTA or the locus coeruleus.
These neuromodulator systems also play a central role in adding new information to the memory trace during its reconsolidation. Again, their requirement upon memory reactivation could be overcome by the previous exploration of a NOF that enables PRPs synthesis.
Taken together, our results position these neuromodulator systems within the reconsolidation BT process as key regulators of PRPs synthesis, crucial for trace stabilization of the original and the newly acquired information.