ArticleFrontiers in behavioral neuroscience2013
Reactivating fear memory under propranolol resets pre-trauma levels of dendritic spines in basolateral amygdala but not dorsal hippocampus neurons.
Article in Frontiers in behavioral neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Propranolol Administration During Morphine Addiction Attenuates Reinstatement of Drug-Aversive Memories Caused by Exposure to Stressful Stimuli.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Memory Impairing Effect of Propranolol on Consolidation and Reconsolidation for Various Learning Tasks.Noro psikiyatri arsivi · 2023Review
- Propranolol versus Other Selected Drugs in the Treatment of Various Types of Anxiety or Stress, with Particular Reference to Stage Fright and Post-Traumatic Stress Disorder.International journal of molecular sciences · 2022Review
- Pharmacological Implications of Adjusting Abnormal Fear Memory: Towards the Treatment of Post-Traumatic Stress Disorder.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Propranolol Administration Modulates Neural Activity in the Hippocampal Hilus During Fear Retrieval.Frontiers in behavioral neuroscience · 2022Article
- Propranolol Decreases Fear Expression by Modulating Fear Memory Traces.Biological psychiatry · 2021Article
- Article
- Parsing differences in amygdala volume among individuals with and without social and generalized anxiety disorders across the lifespan.Journal of psychiatric research · 2020Article
- A brainstem-central amygdala circuit underlies defensive responses to learned threats.Molecular psychiatry · 2020Article
- 5-HTACS chemical neuroscience · 2019Article
- Transcriptional Regulation Involved in Fear Memory Reconsolidation.Journal of molecular neuroscience : MN · 2018Review
- Effects of Propranolol, a β-noradrenergic Antagonist, on Memory Consolidation and Reconsolidation in Mice.Frontiers in behavioral neuroscience · 2016Article
- Pharmacotherapy in the aftermath of trauma; opportunities in the 'golden hours'.Current psychiatry reports · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fear memory enhances connectivity in cortical and limbic circuits but whether treatments disrupting fear reset connectivity to pre-trauma level is unknown. Here we report that C56BL/6J mice exposed to a tone-shock association in context A (conditioning), and briefly re-exposed to the same tone-shock association in context B (reactivation), exhibit strong freezing to the tone alone delivered 48 h later in context B (long term fear memory). This intense fear response is associated with a massive increase in dendritic spines and phospho-Erk (p-ERK) signaling in basolateral amygdala (BLA) but neurons. We then show that propranolol (a central/peripheral β-adrenergic receptor blocker) administered before, but not after, the reactivation trial attenuates long term fear memory assessed drug free 48 h later, and completely prevents the increase in spines and p-ERK signaling in BLA neurons. An increase in spines, but not of p-ERK, was also detected in the dorsal hippocampus (DH) of the conditioned mice. DH spines, however, were unaffected by propranolol suggesting their independence from the ERK/β-ARs cascade. We conclude that propranolol selectively blocks dendritic spines and p-ERK signaling enhancement in the BLA; its effect on fear memory is, however, less pronounced suggesting that the persistence of spines at other brain sites decreases the sensitivity of the fear memory trace to treatments selectively targeting β ARs in the BLA.
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