Article (Scientific journals)
Paroxetine treatment, following behavioral suppression of PTSD-like symptoms in mice, prevents relapse by activating the infralimbic cortex.
Bentefour, Yassine; Rakibi, Youness; Bennis, Mohamed et al.
2016In European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 26 (2), p. 195-207
Peer reviewed
 

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Keywords :
Analysis of Variance; Anesthetics, Local/pharmacology; Animals; Antidepressive Agents, Second-Generation/pharmacology/therapeutic use; Avoidance Learning/drug effects; Cerebral Cortex/drug effects; Conditioning, Classical/drug effects; Cues; Disease Models, Animal; Electroshock/adverse effects; Freezing Reaction, Cataleptic/drug effects; Male; Maze Learning/drug effects; Mice; Oncogene Proteins v-fos/metabolism; Paroxetine/pharmacology/therapeutic use; Recurrence; Stress Disorders, Post-Traumatic/drug therapy; Tetrodotoxin/pharmacology; Time Factors; Antidepressant; Infralimbic cortex; Mouse PTSD model; Relapse prevention
Abstract :
[en] Clinical studies have shown that post-traumatic stress disorder (PTSD) remission, induced by selective serotonin reuptake inhibitor (SSRI) treatment, is associated with increased prefrontal activation during post-treatment symptom provocation. Other studies have shown that continuation SSRI treatment after remitting from PTSD reduces the rate of relapse. The aim of the present preclinical study was to investigate the relationship between post-treatment prefrontal changes and PTSD relapse prevention. Avoidance conditioning (with a 1.5-mA foot-shock), avoidance extinction and a trauma priming exposure (with a 0.3-mA foot-shock) were used in mice to induce, suppress and reactivate PTSD-like symptoms (including avoidance, fear sensitization, enhanced contextual fear, and anxiety-like behavior), respectively. Paroxetine, injected at 8 mg/kg/day (7 days), was used as SSRI treatment. PTSD-like symptoms were present for at least 30 days and resistant to paroxetine treatment. However, after extinction training (suppressing all PTSD-like symptoms), paroxetine treatment prevented symptom reactivation. Paroxetine treatment also induced infralimbic neuronal activation. However, infralimbic functional tetrodotoxin inactivation abolished the preventive effect of paroxetine treatment on symptom reactivation. The data reveal a potential ability of treatments inducing infralimbic activation to provide prophylactic protection against PTSD relapse.
Disciplines :
Anatomy (cytology, histology, embryology...) & physiology
Author, co-author :
Bentefour, Yassine ;  Université de Liège - ULiège > Neurosciences-Neuroendocrinology
Rakibi, Youness
Bennis, Mohamed
Ba-M'hamed, Saadia
Garcia, Rene
Language :
English
Title :
Paroxetine treatment, following behavioral suppression of PTSD-like symptoms in mice, prevents relapse by activating the infralimbic cortex.
Publication date :
2016
Journal title :
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
ISSN :
0924-977X
eISSN :
1873-7862
Volume :
26
Issue :
2
Pages :
195-207
Peer reviewed :
Peer reviewed
Commentary :
Copyright (c) 2015 Elsevier B.V. and ECNP. All rights reserved.
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