Fear Inhibition and Fear Extinction in Post-Traumatic Stress Disorder (PTSD): Novel Findings

2012 ◽  
Author(s):  
Marit Sijbrandij ◽  
Michelle Craske
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Fear Extinction ◽  
Post Traumatic Stress ◽  
Post Traumatic

Cracking the EMDR code: Recruitment of sensory, memory and emotional networks during bilateral alternating auditory stimulation

2020 ◽  
Vol 54 (8) ◽  
pp. 818-831 ◽  
Author(s):  
Pierre-François Rousseau ◽  
Sarah Boukezzi ◽  
René Garcia ◽  
Thierry Chaminade ◽  
Stéphanie Khalfa
Keyword(s):  
Eye Movement ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Conditioned Fear ◽  
Statistical Significance ◽  
Fear Extinction ◽  
Post Traumatic Stress ◽  
The Core ◽  
Post Traumatic

Introduction: The inability to extinguish a conditioned fear is thought to be at the core of post-traumatic stress disorder. Eye movement desensitization and reprocessing therapy has been efficacious for post-traumatic stress disorder, but the brain mechanisms underlying the effect are still unknown. The core effect of eye movement desensitization and reprocessing therapy seems to rely on the simultaneous association of bilateral alternating stimulation and the recall of the traumatic memory. To shed light on how eye movement desensitization and reprocessing therapy functions, we aimed to highlight the structures activated by bilateral alternating stimulation during fear extinction and its recall. Methods: We included 38 healthy participants in this study. Participants were examined twice in functional magnetic resonance imaging, over 2 consecutive days. On the first day, they performed two fear conditioning and extinction procedures, one with and one without the bilateral alternating stimulation during the fear extinction learning phase in a counter-balanced order across the participants. On the second day, participants completed the fear extinction recall procedure, in the same order as the previous day. Statistical significance of maps was set at p < 0.05 after correction for family-wise error at the cluster level. Results: The analysis revealed significant activation with versus without bilateral alternating stimulation at the early extinction in the bilateral auditory areas, the right precuneus, and the left medial frontal gyrus. The same pattern was found in the early recall on the second day. The connectivity analysis found a significant increase in connectivity during bilateral alternating stimulation versus without bilateral alternating stimulation in the early extinction and recall between the two superior temporal gyri, the precuneus, the middle frontal gyrus and a set of structures involved in multisensory integration, executive control, emotional processing, salience and memory. Conclusion: We show for the first time that in the eye movement desensitization and reprocessing therapy the bilateral alternating stimulation is not a simple sensory signal and can activate large emotional neural networks.

scholarly journals Up-Regulation of αCaMKII Impairs Cued Fear Extinction and NMDAR-Dependent LTD in the Lateral Amygdala

2020 ◽  
Author(s):  
Shuming An ◽  
Jiayue Wang ◽  
Xuliang Zhang ◽  
Yanhong Duan ◽  
Junyan Lv ◽  
...  
Keyword(s):  
Normal Level ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Fear Extinction ◽  
Post Traumatic Stress ◽  
Lateral Amygdala ◽  
Molecular Determinant ◽  
Post Traumatic ◽  
First Time

ABSTRACTImpaired fear extinction is one of the hallmark symptoms of post-traumatic stress disorder (PTSD). The roles of αCaMKII have been not extensively studied in fear extinction and LTD. Here, we found PTSD susceptible mice exhibited significant up-regulation of αCaMKII in the lateral amygdala (LA). Consistently, increasing αCaMKII in LA profoundly not only caused PTSD-like symptoms such as impaired fear extinction and anxiety-like behaviors, but also attenuated NMDAR-dependent LTD at thalamo-LA synapses, reduced GluA1-Ser845/Ser831 dephosphorylation and AMPAR internalization. Suppressing the elevated αCaMKII to normal level could completely reverse both PTSD-like symptoms and the impairments in LTD, GluA1-Ser845/Ser831 dephosphorylation and AMPAR internalization. Intriguingly, deficits in AMPAR internalization and GluA1-Ser845/Ser831 dephosphorylation were detected not only after impaired fear extinction, but also after attenuated LTD Our results demonstrate for the first time GluA1-Ser845/Ser831 dephosphorylation and AMPAR internalization are molecular links between LTD and fear extinction, and suggest αCaMKII may be a potential molecular determinant of PTSD.

scholarly journals Clinical Therapeutic Strategy and Neuronal Mechanism Underlying Post-Traumatic Stress Disorder (PTSD)

2019 ◽  
Vol 20 (15) ◽  
pp. 3614 ◽  
Author(s):  
Yasushi Yabuki ◽  
Kohji Fukunaga
Keyword(s):  
Fatty Acid ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Terrorist Attack ◽  
Fear Extinction ◽  
Ptsd Symptoms ◽  
Post Traumatic Stress ◽  
Fatty Acid Binding ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) is characterized by an exaggerated response to contextual memory and impaired fear extinction, with or without mild cognitive impairment, learning deficits, and nightmares. PTSD is often developed by traumatic events, such as war, terrorist attack, natural calamities, etc. Clinical and animal studies suggest that aberrant susceptibility of emotion- and fear-related neurocircuits, including the amygdala, prefrontal cortex (PFC), and hippocampus may contribute to the development and retention of PTSD symptoms. Psychological and pharmacological therapy, such as cognitive behavioral therapy (CBT), and treatment with anti-depressive agents and/or antipsychotics significantly attenuate PTSD symptoms. However, more effective therapeutics are required for improvement of quality of life in PTSD patients. Previous studies have reported that ω3 long-chain polyunsaturated fatty acid (LCPUFA) supplements can suppress the development of PTSD symptoms. Fatty acid binding proteins (FABPs) are essential for LCPUFA intracellular trafficking. In this review, we have introduced Fabp3 null mice as an animal model of PTSD with impaired fear extinction. Moreover, we have addressed the neuronal circuits and novel therapeutic strategies for PTSD symptoms.

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