A hyperexcited basolateral amygdala complex state determines the hippocampal structural plasticity associated with the reconsolidation of a fear memory.

An inadequate response to traumatic experiences due to a loss of plasticity in memory processing could determine the onset of disorders such as post-traumatic stress disorder (PTSD). In this sense, it has been proven that acute stress exposure prior to the encoding of a fear memory alters the plasticity of said memory rendering it unable to undergo a destabilization/reconsolidation process, which is fundamental for memory maintenance and updating. Moreover, it has been shown that inescapable stress induces a hyperexcited state, through loss of GABAergic inhibition in a key structure for fear memory processing such as the basolateral amygdala complex (BLA). In the present study, we sought to elucidate the impact of BLA hyperexcitation, induced by local bicuculline (BIC) infusion, on the hippocampal structural plasticity associated with the destabilization/reconsolidation of contextual fear memories and whether this effect can be prevented or rescued by NMDA receptors modulation. Consistent with previous research, the dendritic spines and behavioural results provide solid evidence that BLA hyperexcitation alters the dorsal hippocampus (DH) involvement in memory reconsolidation in a similar manner to stress exposure. This reinforces the notion that there is a critical interaction between BLA and DH during the processing of this information. In turn, NMDA modulation, through D-cycloserine injection prior to memory reactivation, reverses the effects of BIC infusion. This may be key to identifying new therapeutic targets for the treatment of disorders associated with a maladaptive response to relevant negative emotional events.