There is evidence from animal studies that a memory is not permament but instead is changed and returns to a labile, “supposedly protein synthesis–dependent state,” whenever it is drawn from long-term memory and activated. This process raises the possibility that a beta-adrenegic receptor antagonist such as propranolol could disrupt the reconsolidation of the fear memory and thus eliminate it.
Using a fear-conditioning procedure, Kindt et al recently tested the evidence that propranolol can affect behavioral fear responses after reactivation in humans. They measured the potentation of the eyeblink startle reflex to a loud noise as compared to the reflex to a control stimulus in each subject. The difference in these measures was operationally defined as the level of fear in each subject.
The researchers divided their subjects into two groups (n=20 for each), one of which was given the drug and one of which was given placebo. They ran them on identical procedures, noting that after the acquisition phase both of the groups showed differential responding with more eyeblink startle directed towards the fear-conditioned stimulus.
However, when the extinction trials started 48 hours after the drug was administered, the propanolol group was found to have significantly lower responding to the fear-conditioned stimulus (F(19)=25.47, P<0.001, eta^2 = 0.57), while the placebo group did not (F(19)<1). This suggests that when the memory is reactivated the drug prevents it from being reconsolidated. Using a separate experimental group (n=20), the researchers determined that reactivation of the memory is necessary for the behavioral fear response to be reduced by the drug, suggesting that reconsolidation blocking is the primary mechanism at play.
Kindt M, Soeter M, Vervliet B. Beyond extinction: erasing human fear responses and preventing the return of fear. Nature Neuroscience 12:256-258.doi:10.1038/nn.2271