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Investigating auditory fear memory erasure in the basolateral amygdala


 
 
 
New memories are initially fragile and need protein synthesis in order to be stabilized for long-term storage, a mechanism called cellular consolidation. When recalled, memories are re-activated and become unstable again. They therefore need to be re-stored through a process called reconsolidated. Behavioural studies in rats using auditory fear conditioning have demonstrated that propranolol, a β-adrenergic receptor antagonist, administered following memory reactivation can reduce fear expression (freezing), which has been interpreted as amnesia for the fear memory. It was recently discovered that GluR1-containing AMPA receptors are recruited into the post-synaptic membrane of the basolateral amygdala during auditory fear conditioning, suggesting that synaptic GluR1 increase may be a molecular correlate of long-term memory. The present study aims to investigate what molecular mechanisms accounts for the observed amnesia following a reconsolidation blockade by propranolol. Rats were trained in an auditory fear conditioning task, and fear memory reactivation was followed by systemic propranolol administration. Rats were then euthanized and GluR1 protein levels in baso-lateral amygdala synaptoneurosomes were quantified. We report preliminary evidence to suggest that a reconsolidation blockade by propranolol reduces fear expression with a concomitant reduction in GluR1. Such evidence suggests that a reconsolidation blockade might, at a molecular level, erase a component of the fear memory, providing support for the clinical utility of this treatment for post-traumatic stress disorder. 
 
 
 
