International Society for Traumatic Stress Studies

Student Perspectives The Effect of Beta-Blockers on Traumatic Memory Consolidation and Reconsolidation

Posted 18 November 2014 in StressPoints by Tara Frem, BA

Psychological effects of experiencing a trauma may be reduced through psychopharmacological means by blocking activation of the beta-adrenergic stress system.
 

Previous studies demonstrated that activation of the beta-adrenergic stress hormone system in response to an emotional experience leads to enhanced memory of the event (for review see: McGaugh, 2000). Prolonged adrenergic activity increases fear conditioning and the risk for posttraumatic stress disorder (Orr et al., 2000), as well as the overconsolidation of traumatic memories (Southwick et al., 1999).

Strange and Dolan (2004) demonstrated that though emotional experiences may increase episodic memory formation, administering propranolol (i.e., a beta-blocker) at encoding abolishes the amygdala’s typical action of enhancing encoding and reduces the hippocampus’ retrieval effects.

Propranolol significantly impairs memory of emotionally arousing stimuli, but not of neutral stimuli (Cahill, Prins, Weber, & McGaugh, 1994). McGaugh (2000) reviewed well-established studies that demonstrated the role of propranolol in eliminating the memory enhancement mechanisms, specifically memory consolidation, linked to adrenergic receptors. Beta-blockers were also shown to reduce posttraumatic stress disorder (PTSD) symptomatology (e.g., Pitman et al., 2002; Vaiva et al., 2003). Brunet et al. (2008) maintained that preventing memory consolidation may explain how propranolol reduces the severity of posttraumatic stress disorder.

Not only is propranolol shown to be effective at blocking memory consolidation but also memory reconsolidation. Reactivating a memory by retrieving it makes the memory labile and susceptible to manipulation, also known as reconsolidation (Debiec & Ledoux, 2006). The effect of beta-blockers on memory reconsolidation may be seen as inducing retrograde amnesia for memories of trauma (Diergaarde, Schoffelmeer, & De Vries, 2008).

In 2004, Debiec and Ledoux conducted a study with rats in which they directly injected propranolol into the amygdala, which is responsible for fear encoding. The rats learned a fear conditioning paradigm in which a tone was paired with a foot shock. Administering propranolol post-reactivation of the foot shock memory decreased fear responses (i.e., freezing) measured 48 hours later and two months later, but not three hours after reactivation.

Therefore, administering propranolol during memory reconsolidation was found to impair long-term but not short-term memory. Importantly, Debiec and Ledoux (2004) demonstrated that memory reactivation is necessary for noradrenigc blockade with propranolol. Beta-blockers may be an effective treatment for PTSD, even after the traumatic memory is consolidated, by reactivating the memory and administering propranolol (Debiec & Ledoux, 2006).

In 2008, Brunet et al. conducted a study that demonstrated that participants with PTSD who received propranolol after listening to a recording of their personal trauma narrative and imagining the event showed physiological responses similar to trauma survivors without PTSD (i.e., lower heart rate, skin conductance response, and left corrugator electromyogram) compared to PTSD participants given a placebo. The researchers established that the administration of the beta-blocker accounted for 49 percent of the variance.

A recent meta-analysis by Lonergan, Olivera-Figueroa, Pitman, and Brunet (2013) investigated the role of propranolol on memory consolidation and reconsolidation in healthy participants. They found that the beta-blocker, when given prior to consolidation and reconsolidation, helped reduce later recall of negative stimuli. They maintained that more studies need to be conducted on clinical populations, such as those with PTSD, to determine if the effects of reconsolidation can be achieved on more powerful and personally-meaningful memories.

The link between beta-blockers and memory consolidation and reconsolidation motivates possible future studies involving autobiographical memory specificity. Williams (1996) stated that exposure to trauma leads to overgenerality of memories. To avoid painful memories, blocking autobiographical memory retrieval is necessary to avoid recalling the memory of the traumatic event.

Overgenerality of autobiographical memories was shown to be linked to the development of PTSD (e.g., Harvey, Bryant, & Dang, 1998; Kleim & Ehlers, 2008). Though Williams (1996) and others argued that trauma is the key factor leading to the overgenerality of autobiographical memories, Moore and Zoellner’s (2007) meta-analysis concluded that posttraumatic symptoms, rather than trauma exposure itself, are the key.

Future studies should examine whether beta-blocker administration during traumatic memory reconsolidation can “reverse” the negative effects of trauma on autobiographical memory specificity.

About the Author

Tara Frem, BA, is currently a second-year clinical psychology doctoral student at The Chicago School of Professional Psychology. She is completing her first practicum experience as a diagnostic psychology extern at Sarah’s Circle, a non-profit shelter for homeless women and those looking for a safe space. Tara is interested in the fields of international human rights, military affairs, and traumatic stress.


References

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