Literature DB >> 22445897

Cannabinoid receptors activation and glucocorticoid receptors deactivation in the amygdala prevent the stress-induced enhancement of a negative learning experience.

Assaf Ramot1, Irit Akirav.   

Abstract

The enhancement of emotional memory is clearly important as emotional stimuli are generally more significant than neutral stimuli for surviving and reproduction purposes. Yet, the enhancement of a negative emotional memory following exposure to stress may result in dysfunctional or intrusive memory that underlies several psychiatric disorders. Here we examined the effects of stress exposure on a negative emotional learning experience as measured by a decrease in the magnitude of the expected quantity of reinforcements in an alley maze. In contrast to other fear-related negative experiences, reward reduction is more associated with frustration and is assessed by measuring the latency to run the length of the alley to consume the reduced quantity of reward. We also examined whether the cannabinoid receptors agonist WIN55,212-2 (5 μg/side) and the glucocorticoid receptors (GRs) antagonist RU-486 (10 ng/side) administered into the rat basolateral amygdala (BLA) could prevent the stress-induced enhancement. We found that intra-BLA RU-486 or WIN55,212 before stress exposure prevented the stress-induced enhancement of memory consolidation for reduction in reward magnitude. These findings suggest that cannabinoid receptors and GRs in the BLA are important modulators of stress-induced enhancement of emotional memory.
Copyright © 2012 Elsevier Inc. All rights reserved.

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Year:  2012        PMID: 22445897     DOI: 10.1016/j.nlm.2012.03.003

Source DB:  PubMed          Journal:  Neurobiol Learn Mem        ISSN: 1074-7427            Impact factor:   2.877


  9 in total

Review 1.  Stress modulation of reconsolidation.

Authors:  Irit Akirav; Mouna Maroun
Journal:  Psychopharmacology (Berl)       Date:  2012-10-06       Impact factor: 4.530

2.  Allostatic load and the cannabinoid system: implications for the treatment of physiological abnormalities in post-traumatic stress disorder (PTSD).

Authors:  James B Lohr; Hang Chang; Michelle Sexton; Barton W Palmer
Journal:  CNS Spectr       Date:  2019-07-15       Impact factor: 3.790

Review 3.  Drug discovery strategies that focus on the endocannabinoid signaling system in psychiatric disease.

Authors:  Ryan Wyrofsky; Paul McGonigle; Elisabeth J Van Bockstaele
Journal:  Expert Opin Drug Discov       Date:  2014-12-09       Impact factor: 6.098

4.  Cannabinoids ameliorate impairments induced by chronic stress to synaptic plasticity and short-term memory.

Authors:  Hila Abush; Irit Akirav
Journal:  Neuropsychopharmacology       Date:  2013-02-20       Impact factor: 7.853

5.  Cannabinoids and Glucocorticoids in the Basolateral Amygdala Modulate Hippocampal-Accumbens Plasticity After Stress.

Authors:  Amir Segev; Irit Akirav
Journal:  Neuropsychopharmacology       Date:  2015-08-20       Impact factor: 7.853

6.  Cannabinoid receptor activation prevents the effects of chronic mild stress on emotional learning and LTP in a rat model of depression.

Authors:  Amir Segev; Adva S Rubin; Hila Abush; Gal Richter-Levin; Irit Akirav
Journal:  Neuropsychopharmacology       Date:  2013-10-21       Impact factor: 7.853

7.  Glucocorticoids Interact with Cholinergic System in Impairing Memory Reconsolidation of an Inhibitory Avoidance Task in Mice.

Authors:  Somayeh Amiri; Zahra Jafarian; Abbas Ali Vafaei; Zahra Motaghed-Larijani; Seyed Afshin Samaei; Ali Rashidy-Pour
Journal:  Basic Clin Neurosci       Date:  2015-07

Review 8.  Nightmares and the Cannabinoids.

Authors:  Mortimer Mamelak
Journal:  Curr Neuropharmacol       Date:  2020       Impact factor: 7.363

Review 9.  Single-Prolonged Stress: A Review of Two Decades of Progress in a Rodent Model of Post-traumatic Stress Disorder.

Authors:  Michael J Lisieski; Andrew L Eagle; Alana C Conti; Israel Liberzon; Shane A Perrine
Journal:  Front Psychiatry       Date:  2018-05-15       Impact factor: 4.157

  9 in total

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