Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

1.3K
β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in...
1.3K
Role of Amygdala in Memory01:16

Role of Amygdala in Memory

641
The amygdala is a small, almond-shaped structure responsible for processing and storing memories, particularly those linked to emotions like fear and stress. It plays an essential role in the brain's response to emotionally significant events and often enhances memory formation by triggering stress hormone release. The amygdala is vital for encoding and retrieving memories associated with fear or stress, a process that is adaptive by helping organisms avoid dangerous situations.
One of the...
641
Antihypertensive Drugs: Types of β-Blockers01:28

Antihypertensive Drugs: Types of β-Blockers

1.2K
β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and...
1.2K
Anxiolytic Drugs: Overview01:26

Anxiolytic Drugs: Overview

731
Anxiolytic drugs are vital in managing anxiety disorders by effectively alleviating symptoms such as excessive fear, tachycardia, and tremors. There are several classes of anxiolytic medications, each with unique mechanisms of action and potential side effects.
Primary Types of Anxiolytic Drugs
1. Benzodiazepines:
Benzodiazepines bind to the GABA-A receptor in the brain, enhancing GABA's interaction. This action reduces neurotransmission, effectively blocking anxiety-associated limbic...
731
Behavior Therapy01:22

Behavior Therapy

274
Behavior therapy incorporates diverse techniques rooted in classical conditioning principles to address maladaptive behaviors and anxiety disorders. These methods aim to reduce avoidance behaviors, foster adaptive coping mechanisms, and alter associations between stimuli and responses, making them effective in a wide range of therapeutic contexts.
Exposure therapy is a cornerstone of behavioral treatment for anxiety disorders. It involves systematic exposure to feared stimuli, either in real...
274
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

1.1K
Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
1.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Medial entorhinal-hippocampal desynchronization parallels the emergence of memory impairment in a mouse model of Alzheimer's disease pathology.

Cell reports·2026
Same author

Altered striatal dopamine regulation in Adgrl3 knockout mice.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology·2026
Same author

Prucalopride, a serotonin type 4 receptor agonist, induces fast anxiolytic/antidepressant effects and concomitant changes in the gut microbiota.

NPJ biofilms and microbiomes·2026
Same author

Maladaptive immunity to the microbiota promotes neuronal hyperinnervation and itch via IL-17A.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

Novel, small molecules targeting the 5-HT<sub>4</sub> receptor protect against stress-induced maladaptive behavior with efficacy across age.

bioRxiv : the preprint server for biology·2025
Same author

Immediate-early genes Arc and c-Fos show divergent brain-wide expression following contextual fear conditioning.

Communications biology·2025

Related Experiment Video

Updated: Nov 11, 2025

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic &#946;-Blocker
08:32

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

23.1K

Propranolol Decreases Fear Expression by Modulating Fear Memory Traces.

Sofia Leal Santos1, Michelle Stackmann2, Andrea Muñoz Zamora3

  • 1Department of Psychiatry, Columbia University Irving Medical Center, New York, New York; Division of Systems Neuroscience, Research Foundation for Mental Hygiene Inc/New York State Psychiatric Institute, New York, New York; Life and Health Sciences Research Institute, School of Medicine, University of Minho, Braga, Portugal; ICVS/3B's - PT Government Associate Laboratory, Braga, Portugal.

Biological Psychiatry
|March 26, 2021
PubMed
Summary

Propranolol reduces fear in posttraumatic stress disorder (PTSD) by altering brain activity and weakening traumatic memory traces when given before reexposure. This offers a new therapeutic approach for PTSD.

Keywords:
ArcContextual fear conditioningEngramMemoryPropranololTracec-Fos

More Related Videos

Extinction Training During the Reconsolidation Window Prevents Recovery of Fear
11:17

Extinction Training During the Reconsolidation Window Prevents Recovery of Fear

Published on: August 24, 2012

35.8K
Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats
13:38

Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats

Published on: August 22, 2020

8.5K

Related Experiment Videos

Last Updated: Nov 11, 2025

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic &#946;-Blocker
08:32

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

23.1K
Extinction Training During the Reconsolidation Window Prevents Recovery of Fear
11:17

Extinction Training During the Reconsolidation Window Prevents Recovery of Fear

Published on: August 24, 2012

35.8K
Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats
13:38

Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats

Published on: August 22, 2020

8.5K

Area of Science:

  • Neuroscience
  • Pharmacology
  • Psychiatry

Background:

  • Posttraumatic stress disorder (PTSD) affects 8% of the U.S. population, with limited FDA-approved treatments.
  • Propranolol, a beta-blocker, shows promise in treating exaggerated fear responses.
  • Understanding propranolol's mechanism in fear attenuation is crucial for developing effective PTSD therapies.

Purpose of the Study:

  • To investigate the neurobiological mechanisms by which propranolol reduces fear.
  • To determine how propranolol affects memory traces in key brain regions involved in fear.
  • To explore propranolol's impact on functional connectivity in fear networks.

Main Methods:

  • Utilized an activity-dependent tagging system (ArcCreERT2 x eYFP mice) to track neuronal ensembles.
  • Administered propranolol or saline before contextual fear conditioning and reexposure paradigms.
  • Quantified fear memory traces in the hippocampus, prefrontal cortex, and amygdala.

Main Results:

  • Propranolol significantly decreased fear expression only when administered before delayed context reexposure.
  • Fear memory traces were altered in the dorsal dentate gyrus and basolateral amygdala post-propranolol.
  • Propranolol acutely modulated functional connectivity within the hippocampal-cortical-amygdalar network.

Conclusions:

  • Propranolol may reduce PTSD symptoms by disrupting traumatic memory reactivation and altering network activity.
  • Findings support the potential of noradrenergic drugs like propranolol as therapeutic agents for PTSD.
  • This research provides insight into the neural basis of fear memory and its modulation.