Research article summary (published 30 Dec 2003):

The inhibition of acquired fear.

Full Abstract

A conditioned stimulus (CS) associated with a fearsome unconditioned stimulus (US) generates learned fear. Acquired fear is at the root of a variety of mental disorders, among which phobias, generalized anxiety, the posttraumatic stress disorder (PTSD) and some forms of depression. The simplest way to inhibit learned fear is to extinguish it, which is usually done by repeatedly presenting the CS alone, so that a new association, CS-"no US", will eventually overcome the previously acquired CS-US association. Extinction was first described by Pavlov as a form of "internal inhibition" and was recommended by Freud and Ferenczi in the 1920s (who called it "habituation") as the treatment of choice for phobic disorders. It is used with success till this day, often in association with anxiolytic drugs. Extinction has since then been applied, also successfully and also often in association with anxiolytics, to the treatment of panic, generalized anxiety disorders and, more recently, PTSD. Extinction of learned fear involves gene expression, protein synthesis, N-methyl-D-aspartate (NMDA) receptors and signaling pathways in the hippocampus and the amygdala at the time of the first CS-no US association. It can be enhanced by increasing the exposure to the "no US" component at the time of behavioral testing, to the point of causing the complete uninstallment of the original fear response. Some theorists have recently proposed that reiteration of the CS alone may induce a reconsolidation of the learned behavior instead of its extinction. Reconsolidation would preserve the original memory from the labilization induced by its retrieval. If true, this would of course be disastrous for the psychotherapy of fear-motivated disorders. Here we show that neither the CS nor retrieval cause anything remotely like reconsolidation, but just extinction. In fact, our findings indicate that the reconsolidation hypothesis is essentially incorrect, at least for the form of contextual fear most commonly studied in rodents. Therefore, it seems safe to continue using extinction-based forms of therapy for disorders secondary to acquired fear. Further, it is useful and desirable to device procedures by which the "no US" component of the extinction is strengthened in order to alleviate the symptoms of victims of acquired fear.

Author information

Author/s: Izquierdo, Iván (I); Cammarota, Martín (M); Vianna, Mónica M R (MM); Bevilaqua, Lía R M (LR);

Affiliation: Centro de Memoria, ICBS, Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos 2600--Anexo, Porto Alegre, RS 90035-003, Brasil. izquier(-atsign-)terra.com.br

Journal and publication information

Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

Journal: Neurotoxicity research (Neurotox Res), published in United States. (Language: eng)

Reference: 2004-; vol 6 (issue 3) : pp 175-88

Dates: Created 2004/08/24; Completed 2005/01/31; Revised 2006/11/15;

PMID: 15325957, status: MEDLINE (last retrieved date: 2/18/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Adrenocorticotropic Hormone - pharmacology Animals Avoidance Learning - physiology Behavior, Animal Brain - anatomy & histology; drug effects Conditioning, Classical - drug effects; physiology Endocannabinoids - pharmacology Enzyme Inhibitors - pharmacology Extinction, Psychological - drug effects

Fear - drug effects; physiology Inhibition (Psychology) Mental Recall - drug effects Norepinephrine - pharmacology Rats Reaction Time - drug effects Retention (Psychology) - drug effects Statistics, Nonparametric Time Factors

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Endocannabinoids (0) ; Enzyme Inhibitors (0) ; Norepinephrine (51-41-2) ; Adrenocorticotropic Hormone (9002-60-2)

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