How can beta-adrenergic antagonists be used for the disruption of re-consolidation of memories? - Kindt et al. - 2009 - Article


Can we change emotional memories in animals?

Emotional memories seem ineffaceable, which is harmful when someone has experienced trauma. Treatments have mainly focused on eliminating fearful responding. However, this leaves the original memory of the trauma intact and can lead to many relapses. Weakening or erasing a memory could prevent the development of a post-traumatic stress disorder. In animal research, it was found that memories can be changed. After reactivating a memory, it becomes labile. Neurobiological manipulations during or briefly after reactivation can alter protein synthesis directly or by interaction with neurotransmitter secretion in the amygdala. This changes expressions of the memory. An example of such a manipulation is the infusion of propranolol in the amygdala, which disrupts the reconsolidation process of a reactivated memory. The basolateral amygdala is important in fear memories.

Can the disruption of reconsolidation change fear memories in humans?

The current study included three different stages:

  1. Fear acquisition;
  2. Reactivation of the fear memory;
  3. Extinction, reinstatement procedure and test phase.

One group of people was administered propranolol before memory reactivation and another group got a placebo. The study found no differences in fear learning or startle response during reactivation of the fear memory between the two groups. Propranolol did not directly influence how a fear memory was expressed. However, propranolol administration did weaken the fear response, as the fear expression was eliminated 24 hours later, after only one reactivation trial. Subsequently retrieving the memory by a reinstatement technique did not lead to a fear response. Therefore, the memory was either erased (storage theory) or not available as retrieval was not possible (retrieval theory).

What is the role of β-adrenergic receptors?

Administration of propranolol did not affect the declarative memory. This means that the connection between the conditioned and unconditioned stimulus was still recognized, but no longer led to an emotional reaction. Propranolol affects the β-adrenergic receptors in the amygdala when processing emotional information. Perhaps, blocking these receptors during reconsolidation could intervene in the protein synthesis of a fear memory in the amygdala and thus deconsolidating the fear memory trace. The declarative memory in the hippocampus, however, would remain intact. Concluding, the β-adrenergic receptors are important in reconsolidating conditioned fear memories. Disrupting this reconsolidation process ensures that the fear response is eliminated.

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