The retrieval of a consolidated memory results into a labile phase, vulnerable to interference by benzodiazepines. In a recent study we demonstrate that previous stress induced a memory resistant to reconsolidation after retrieval and D-cycloserine (DCS) prior to reactivation promotes retrieval-induced lability. This suggests that previous stress could be a boundary condition and the participation of NR2B subunit in this process.
The aim of the present study was to characterize, at a molecular level, this boundary condition. Male Wistar rats were subjected on day 1 to a stressfull session then on day 2 were submitted to a contextual fear conditioning paradigm and 7 days after training re-exposed to the training context for 3 min. Thirty minutes after retrieval rats were killed, transcardially perfused and their brains were processed for immunohistochemistry (IHC).
The results showed that NR2B expression in the LBA and hippocampus, which is critical for the induction of fear reconsolidation, was reduced in stressed animals after a reactivation session.
Our evidence showed that: a) Previous stress represent a real boundary condition and b) NR2B NMDA-receptor subunits are critical for the induction of reactivation-reconsolidation of contextual fear memories in the amygdala,
