Trauma Reactivation Under the Influence of Propranolol Decreases Posttraumatic Stress Symptoms and Disorder

Brunet, Alain; Poundja, Joaquin; Tremblay, Jacques; Bui, Éric; Thomas, Émilie; Orr, Scott P.; Azzoug, Abdelmadjid; Birmes, Philippe; Pitman, Roger K.

doi:10.1097/jcp.0b013e318222f360

Cited by 327 publications

(136 citation statements)

References 11 publications

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“…Moreover, these physiologic responses were reduced below threshold for PTSD diagnoses (Brunet et al, 2008). When administered in conjunction with multiple (6) memory reactivation sessions, propranolol treatment reduced the diagnosis of PTSD by more than 70% and reduced symptom severity by more than 50% (Brunet et al, 2011). Finally, propranolol treatment during memory retrieval was associated with improved quality of life and reduced depressive symptoms among patients with PTSD (Poundja et al, 2012).…”

Section: Clinical Trialsmentioning

confidence: 85%

Noradrenergic Regulation of Fear and Drug-Associated Memory Reconsolidation

Otis

Werner

Mueller

2014

Neuropsychopharmacol

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Emotional and traumatic experiences lead to the development of particularly strong memories that can drive neuropsychiatric disorders, such as posttraumatic stress disorder (PTSD) and drug addiction. Disruption of these memories would therefore serve as a powerful treatment option, and targeting the pathologic emotional, but not declarative, component of a memory would be ideal for clinical intervention. Research reveals that after retrieval of a consolidated memory, the memory can be destabilized, and must then be reconsolidated through synaptic plasticity to allow subsequent retrieval. Disruption of reconsolidation-related plasticity would therefore impair specific, reactivated memories. Noradrenergic signaling strengthens synaptic plasticity and is essential for encoding the emotional components of memory. Consistent with this, investigations have now revealed that noradrenergic signaling is a critical mechanism for reconsolidation of emotional memories in rodent and human models. Here, we discuss these investigations and promising clinical trials indicating that disruption of noradrenergic signaling during reconsolidation may abolish the pathologic emotional, but not declarative, component of memories allowing alleviation of neuropsychiatric disorders including PTSD and drug addiction.

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Section: Clinical Trialsmentioning

confidence: 85%

Noradrenergic Regulation of Fear and Drug-Associated Memory Reconsolidation

Otis

Werner

Mueller

2014

Neuropsychopharmacol

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“…We found 10 studies using propranolol in PTSD populations: 4 examined consolidation blockade, 26-29 2 examined reconsolidation blockade, 17,30 and the remaining 4 used propranolol for other unrelated purposes. Owing to insufficient numbers and clinical heterogeneity, we could not include studies focusing on consolidation or reconsolidation blockade as a treatment for PTSD in this meta-analysis.…”

Section: Inclusion Criteriamentioning

confidence: 99%

“…Anecdotally, all the participants of that study retained a declarative memory of their traumatic event. Furthermore, in 3 open-label trials, 1 of which included a control group, Brunet and colleagues 30 demonstrated that 6 treatment sessions with propranolol administered before trauma memory reactivation led to a significant decrease in PTSD symptoms. Propranolol's capacity to prevent the development of PTSD immediately after trauma exposure has also been examined in a few studies with conflicting findings and methodological flaws.…”

Section: Can Propranolol Effectively Block Memory Consolidation or Rementioning

confidence: 99%

Propranolol’s effects on the consolidation and reconsolidation of long-term emotional memory in healthy participants: a meta-analysis

Lonergan

Olivera-Figueroa

Pitman

et al. 2013

J Psychiatry Neurosci

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192

127

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“…This treatment has worked in animal models (e.g. contextual fear; Abrari et al, 2008;Debiec and Ledoux, 2004) and in some cases in humans suffering from PTSD (Pitman et al, 2002;Pitman and Delahanty, 2005;Brunet et al, 2008Brunet et al, , 2011Soeter and Kindt, 2011;Kindt and Soeter, 2013). However, more recent, larger studies have not found a significant effect of propranolol administration after trauma (Sharp et al, 2010;Parsons and Ressler, 2013).…”

Section: Introductionmentioning

confidence: 99%

Sequential exposure to a combination of stressors blocks memory reconsolidation in Lymnaea

Dodd

Lukowiak

2015

Journal of Experimental Biology

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Stress alters the formation of long-term memory (LTM) in Lymnaea. When snails are exposed to more than one stressor, however, how the memory is altered becomes complicated. Here, we investigated how multiple stressors applied in a specific pattern affect an aspect of memory not often studied in regards to stress -reconsolidation. We hypothesized that the application of a sequence of stressors would block the reconsolidation process. Reconsolidation occurs following activation of a previously formed memory. Sequential crowding and handling were used as the stressors to block reconsolidation. When the two stressors were sequentially presented immediately following memory activation, reconsolidation was blocked. However, if the sequential presentation of the stressors was delayed for 1 h after memory activation, reconsolidation was not blocked. That is, LTM was observed. Finally, presentation of either stressor alone did not block reconsolidation. Thus, stressors can block reconsolidation, which may be preferable to pharmacological manipulations.

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Trauma Reactivation Under the Influence of Propranolol Decreases Posttraumatic Stress Symptoms and Disorder

Cited by 327 publications

References 11 publications

Noradrenergic Regulation of Fear and Drug-Associated Memory Reconsolidation

Noradrenergic Regulation of Fear and Drug-Associated Memory Reconsolidation

Propranolol’s effects on the consolidation and reconsolidation of long-term emotional memory in healthy participants: a meta-analysis

Sequential exposure to a combination of stressors blocks memory reconsolidation in Lymnaea

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