title: Revisiting propranolol and PTSD: Memory erasure or extinction enhancement?
abstract: Posttraumatic stress disorder (PTSD) has been described as the only neuropsychiatric disorder with a known cause, yet effective behavioral and pharmacotherapies remain elusive for many afflicted individuals. PTSD is characterized by heightened noradrenergic signaling, as well as a resistance to extinction learning. Research aimed at promoting more effective treatment of PTSD has focused on memory erasure (disrupting reconsolidation) and/or enhancing extinction retention through pharmacological manipulations. Propranolol, a β-adrenoceptor antagonist, has received considerable attention for its therapeutic potential in PTSD, although its impact on patients is not always effective. In this review, we briefly examine the consequences of β-noradrenergic manipulations on both reconsolidation and extinction learning in rodents and in humans. We suggest that propranolol is effective as a fear-reducing agent when paired with behavioral therapy soon after trauma when psychological stress is high, possibly preventing or dampening the later development of PTSD. In individuals who have already suffered from PTSD for a significant period of time, propranolol may be less effective at disrupting reconsolidation of strong fear memories. Also, when PTSD has already developed, chronic treatment with propranolol may be more effective than acute intervention, given that individuals with PTSD tend to experience long-term, elevated noradrenergic hyperarousal.
authors.affiliation: Department of Psychology, Texas A&M University, College Station, TX 77843-3474, United States; Institute for Neuroscience, Texas A&M University, College Station, TX 77843-3474, United States.
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Giustino
authors.affiliation: Department of Psychology, Texas A&M University, College Station, TX 77843-3474, United States.
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.affiliation: Department of Psychology, Texas A&M University, College Station, TX 77843-3474, United States; Institute for Neuroscience, Texas A&M University, College Station, TX 77843-3474, United States.
authors.forename: Stephen
authors.initials: S
authors.lastname: Maren
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D004195:Disease Models, Animal; D005108:Extinction, Psychological / Q000187:drug effects*; D005239:Fear / Q000187:drug effects*; D006801:Humans; D008568:Memory / Q000187:drug effects*; D011433:Propranolol / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D013313:Stress Disorders, Post-Traumatic / Q000188:drug therapy* / Q000523:psychology
chemical_list: D000319:Adrenergic beta-Antagonists; D011433:Propranolol
keywords: Consolidation; Extinction; Fear; Norepinephrine; PTSD; Propranolol; Reconsolidation