scholarly journals Post-acquisition CO2 Inhalation Enhances Fear Memory and Depends on ASIC1A

2021 ◽  
Vol 15 ◽  
Author(s):  
Rebecca J. Taugher ◽  
Amanda M. Wunsch ◽  
Grace Z. Wang ◽  
Aubrey C. Chan ◽  
Brian J. Dlouhy ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Retrieval ◽  
Traumatic Event ◽  
Fear Memory ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Reduce Risk ◽  
Subsequent Modification

A growing body of evidence suggests that memories of fearful events may be altered after initial acquisition or learning. Although much of this work has been done in rodents using Pavlovian fear conditioning, it may have important implications for fear memories in humans such as in post-traumatic stress disorder (PTSD). A recent study suggested that cued fear memories, made labile by memory retrieval, were made additionally labile and thus more vulnerable to subsequent modification when mice inhaled 10% carbon dioxide (CO2) during retrieval. In light of this finding, we hypothesized that 10% CO2 inhalation soon after fear acquisition might affect memory recall 24 h later. We found that both cue and context fear memory were increased by CO2 exposure after fear acquisition. The effect of CO2 was time-dependent, as CO2 inhalation administered 1 or 4 h after cued fear acquisition increased fear memory, whereas CO2 inhalation 4 h before or 24 h after cued fear acquisition did not increase fear memory. The ability of CO2 exposure following acquisition to enhance fear memory was not a general consequence of stress, as restraining mice after acquisition did not alter cued fear memory. The memory-enhancing action of CO2 may be relatively specific to fear conditioning as novel object recognition was impaired by post-training CO2 inhalation. To explore the molecular underpinnings of these effects, we tested if they depended on the acid-sensing ion channel-1a (ASIC1A), a proton-gated cation channel that mediates other effects of CO2, likely via its ability to sense acidosis induced during CO2 inhalation. We found that CO2 inhalation did not alter cued or context fear memory in Asic1a–/– mice, suggesting that this phenomenon critically depends on ASIC1A. These results suggest that brain acidosis around the time of a traumatic event may enhance memory of the trauma, and may thus constitute an important risk factor for developing PTSD. Moreover, preventing peritraumatic acidosis might reduce risk of PTSD.

scholarly journals Electroconvulsive Shock Does Not Impair the Reconsolidation of Cued and Contextual Pavlovian Threat Memory

2020 ◽  
Vol 21 (19) ◽  
pp. 7072
Author(s):  
Hajira Elahi ◽  
Veronica Hong ◽  
Jonathan E. Ploski
Keyword(s):  
Electroconvulsive Shock ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Retrieval ◽  
Memory Trace ◽  
Stress Disorder ◽  
Fear Memory ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Electroconvulsive Seizure

Existing memories, when retrieved under certain circumstances, can undergo modification through the protein synthesis-dependent process of reconsolidation. Disruption of this process can lead to the weakening of a memory trace, an approach which is being examined as a potential treatment for disorders characterized by pathological memories, such as Post-Traumatic Stress Disorder. The success of this approach relies upon the ability to robustly attenuate reconsolidation; however, the available literature brings into question the reliability of the various drugs used to achieve such a blockade. The identification of a drug or intervention that can reliably disrupt reconsolidation without requiring intracranial access for administration would be extremely useful. Electroconvulsive shock (ECS) delivered after memory retrieval has been demonstrated in some studies to disrupt memory reconsolidation; however, there exists a paucity of literature characterizing its effects on Pavlovian fear memory. Considering this, we chose to examine ECS as an inexpensive and facile means to impair reconsolidation in rats. Here we show that electroconvulsive seizure induction, when administered after memory retrieval, (immediately, after 30 min, or after 1 h), does not impair the reconsolidation of cued or contextual Pavlovian fear memories. On the contrary, ECS administration immediately after extinction training may modestly impair the consolidation of fear extinction memory.

scholarly journals Npas4 impairs fear memory via phosphorylated HDAC5 induced by CGRP administration in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Narumi Hashikawa-Hobara ◽  
Shuta Mishima ◽  
Chihiro Okujima ◽  
Youdai Shitanishi ◽  
Naoya Hashikawa
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Histone H3 ◽  
Fear Memory ◽  
Protein Kinase D ◽  
Post Traumatic Stress ◽  
Calcitonin Gene ◽  
Post Traumatic ◽  
H3 Acetylation

AbstractThe relationships among neuropeptide, calcitonin gene-related peptide (CGRP), and memory formation remain unclear. Here, we showed that the intracerebroventricular administration of CGRP impaired the traumatic fear memories, in a widely studied animal model of post-traumatic stress disorder. We found that CGRP administration suppressed fear memory by increasing neuronal PAS domain protein 4 (Npas4), phosphorylated histone deacetylase 5 (HDAC5), and protein kinase D (PKD). We also discovered that Npas4 knockdown inhibited CGRP-mediated fear memory. CGRP decreased the binding between HDAC5 and the Npas4 enhancer site and increased the binding between acetylated histone H3 and the Npas4 enhancer site. The pharmacological inhibition or knockdown of PKD attenuated the CGRP-mediated impairment of fear memory and the increased phosphorylation of HDAC5 and Npas4 expression. Our findings demonstrated that the CGRP-PKD pathway was associated with the histone H3 acetylation-Npas4 pathway. These results suggested a novel function for CGRP on fear memory, through epigenetic regulation.

Support for the mutual maintenance of pain and post-traumatic stress disorder symptoms

2009 ◽  
Vol 40 (7) ◽  
pp. 1215-1223 ◽  
Author(s):  
A. Liedl ◽  
M. O'Donnell ◽  
M. Creamer ◽  
D. Silove ◽  
A. McFarlane ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Structural Equation ◽  
Stress Disorder ◽  
Traumatic Event ◽  
Saturated Model ◽  
Post Traumatic Stress ◽  
Post Injury ◽  
Post Traumatic ◽  
The Relationship

BackgroundPain and post-traumatic stress disorder (PTSD) are frequently co-morbid in the aftermath of a traumatic event. Although several models attempt to explain the relationship between these two disorders, the mechanisms underlying the relationship remain unclear. The aim of this study was to investigate the relationship between each PTSD symptom cluster and pain over the course of post-traumatic adjustment.MethodIn a longitudinal study, injury patients (n=824) were assessed within 1 week post-injury, and then at 3 and 12 months. Pain was measured using a 100-mm Visual Analogue Scale (VAS). PTSD symptoms were assessed using the Clinician-Administered PTSD Scale (CAPS). Structural equation modelling (SEM) was used to identify causal relationships between pain and PTSD.ResultsIn a saturated model we found that the relationship between acute pain and 12-month pain was mediated by arousal symptoms at 3 months. We also found that the relationship between baseline arousal and re-experiencing symptoms, and later 12-month arousal and re-experiencing symptoms, was mediated by 3-month pain levels. The final model showed a good fit [χ2=16.97, df=12, p>0.05, Comparative Fit Index (CFI)=0.999, root mean square error of approximation (RMSEA)=0.022].ConclusionsThese findings provide evidence of mutual maintenance between pain and PTSD.

scholarly journals Prevalence of Post Traumatic Stress Disorder among School-age Adolescent

2020 ◽  
pp. 40-49
Author(s):  
Khalid Astitene ◽  
Hassan Aguenaou ◽  
Laila Lahlou ◽  
Amina Barkat
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Traumatic Event ◽  
Demographic Data ◽  
Post Traumatic Stress ◽  
Cross Sectional ◽  
Reaction Index ◽  
High Prevalence ◽  
Post Traumatic

Aim: After a traumatic event, the person can develop post-traumatic stress disorder (PTSD), the purpose of the study is to assess the prevalence of PTSD in adolescents in public middle schools of the prefecture of Salé in Morocco and study anxiety and depression which are the comorbid disorders of the PTSD. The survey was carried out from March to June 2017. Methods: 523 students were selected by the cross-sectional method from fifteen schools that were randomly selected, the age of the students vary between 12 and 17 years. For the survey, standardized questionnaires (the socio-demographic data, the Life Events Checklist, the CPTS-RI (Children's Post Traumatic Stress Reaction Index), the STAIY (State Trait Inventory Anxiety Form Y) and the CDI (Children Depression Inventory) were used which were filled in by the students. Results: The prevalence of PTSD was 70.4% in the students who have PTSD. We found that the prevalence in boys was 46.74%, while in girls it was 53.26%. In addition to that, 81% of students found to be anxious and 51.8% of students have depression. Conclusion: There is a high prevalence of post traumatic stress disorder among adolescents, there are practical implications for the support and care of these adolescents.

scholarly journals Npas4 impairs fear memory via phosphorylated HDAC5 induced by CGRP administration in mice

2020 ◽  
Author(s):  
Narumi Hashikawa-Hobara ◽  
Shuta Mishima ◽  
Chihiro Okujima ◽  
Youdai Shitanishi ◽  
Naoya Hashikawa
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Histone H3 ◽  
Fear Memory ◽  
Protein Kinase D ◽  
Post Traumatic Stress ◽  
Calcitonin Gene ◽  
Post Traumatic ◽  
H3 Acetylation

Abstract The relationships among neuropeptide, calcitonin gene-related peptide (CGRP), and memory formation remain unclear. Here, we showed that the intracerebroventricular administration of CGRP impaired the traumatic fear memories, in a widely studied animal model of post-traumatic stress disorder. We found that CGRP administration suppressed fear memory by increasing neuronal PAS domain protein 4 (Npas4), phosphorylated histone deacetylase 5 (HDAC5), and protein kinase D (PKD). We also discovered that Npas4 knockdown inhibited CGRP-mediated fear memory. CGRP decreased the binding between HDAC5 and the Npas4 enhancer site and increased the binding between acetylated histone H3 and the Npas4 enhancer site. The pharmacological inhibition or knockdown of PKD attenuated the CGRP-mediated impairment of fear memory and the increased phosphorylation of HDAC5 and Npas4 expression. Our findings demonstrated that the CGRP-PKD pathway was associated with the histone H3 acetylation-Npas4 pathway. These results suggested a novel function for CGRP on fear memory, through epigenetic regulation.

Clinicians after the suicide of their patients

2021 ◽  
pp. 549-554
Author(s):  
Onja T. Grad
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Traumatic Event ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Past Experiences ◽  
Suicidal Patients

Emotional turmoil, disruption, shock, post-traumatic stress disorder (PTSD), doubts in own competences as a professional: these are only few of many feelings and reactions that clinicians might experience when faced with the fact that patients they had treated took their lives. The range of reactions can span from none, which is rare, to severe disorders, and can sometimes result in more precautious treatment of future patients, or even in leaving the field of working with suicidal patients. How clinicians respond depends on many factors, such as the length and intensity of the treatment, the understanding of patients’ suicide, the knowledge and past experiences the clinicians have as well as the response of the patients’ family, and the response and support of the colleagues and the institution in which the treatment took place. Some of these factors can help—while others can hinder—the process of overcoming the traumatic event of patients’ suicide.

scholarly journals Psychological sequelae of political imprisonment, specifically post-traumatic stress disorder, in 491 Days by Winnie Madikizela-Mandela

Literator ◽  
2018 ◽  
Vol 39 (1) ◽  
Author(s):  
Marisa Botha
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Traumatic Event ◽  
Traumatic Experiences ◽  
Post Traumatic Stress ◽  
Psychological Sequelae ◽  
Main Cluster ◽  
Post Traumatic ◽  
Political Imprisonment

This article analyses well-known anti-apartheid activist Winnie Madikizela-Mandela’s prison memoir 491 Days: Prisoner Number 1323/69 (2013) for depictions of suffering. This memoir reveals aspects of politically inflicted trauma, particularly the suffering sustained in prolonged solitary confinement and the resulting psychological sequelae for the prisoner. To move beyond a vague understanding of her traumatic experiences, this article draws on the field of psychiatry, specifically the diagnostic criteria for post-traumatic stress disorder (PTSD) to gain greater insight as this tool may also be regarded as a type of narrative that could aid in the comprehension of traumatic events. References will be made to the three main cluster symptoms of PTSD: involuntary re-experiencing of the traumatic event, avoidance of reminders and an ongoing sense of threat. An interdisciplinary literary-psychological approach will probably lead to a deeper understanding of the mental consequences of political imprisonment, as PTSD was not an acknowledged disorder during Madikizela-Mandela’s detainment.

Effects of cortisol on memory in women with borderline personality disorder: role of co-morbid post-traumatic stress disorder and major depression

2012 ◽  
Vol 43 (3) ◽  
pp. 495-505 ◽  
Author(s):  
K. Wingenfeld ◽  
M. Driessen ◽  
K. Terfehr ◽  
N. Schlosser ◽  
S. Carvalho Fernando ◽  
...  
Keyword(s):  
Working Memory ◽  
Personality Disorder ◽  
Autobiographical Memory ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Retrieval ◽  
Stress Disorder ◽  
Borderline Personality ◽  
Post Traumatic Stress ◽  
Post Traumatic

BackgroundStress and cortisol administration are known to have impairing effects on memory retrieval in healthy humans. These effects are reported to be altered in patients with major depressive disorder (MDD) and post-traumatic stress disorder (PTSD) but they have not yet been investigated in borderline personality disorder (BPD).MethodIn a placebo-controlled cross-over study, 71 women with BPD and 40 healthy controls received either placebo or 10 mg of hydrocortisone orally before undertaking a declarative memory retrieval task (word list learning) and an autobiographical memory test (AMT). A working memory test was also applied.ResultsOverall, opposing effects of cortisol on memory were observed when comparing patients with controls. In controls, cortisol had impairing effects on memory retrieval whereas in BPD patients cortisol had enhancing effects on memory retrieval of words, autobiographical memory and working memory. These effects were most pronounced for specificity of autobiographical memory retrieval. Patients with BPD alone and those with co-morbid PTSD showed this effect. We also found that co-morbid MDD influenced the cortisol effects: in this subgroup (BPD + MDD) the effects of cortisol on memory were absent.ConclusionsThe present results demonstrate beneficial effects of acute cortisol elevations on hippocampal-mediated memory processes in BPD. The absence of these effects in patients with co-morbid MDD suggests that these patients differ from other BPD patients in terms of their sensitivity to glucocorticoids (GCs).

Behavioral Neuroscience of Circuits Involved in Fear Processing

2016 ◽  
Author(s):  
Elizabeth P. Bauer ◽  
Denis Paré
Keyword(s):  
Fear Conditioning ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Current Knowledge ◽  
Brain Structures ◽  
Fear Learning ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Brain ◽  
Insight Into

Normal fear regulation includes the ability to learn by experience that some circumstances predict danger. This process, which can be modeled in the laboratory using Pavlovian fear conditioning, appears to be disrupted in individuals with post-traumatic stress disorder (PTSD). Understanding of the mechanisms underlying fear learning has progressed tremendously in the last 25 years, and constitutes a promising paradigm to study the neural bases of PTSD. This chapter first reviews current knowledge of the brain structures involved in fear learning, expression and extinction, including the contributions of the amygdala and prefrontal cortex. It then addresses how these circuits are affected by PTSD and how fear processing is altered in PTSD. Understanding PTSD within a fear-conditioning and extinction framework provides insight into why certain individuals are susceptible to developing PTSD and suggests potential therapies.

scholarly journals The Pathways between Cortisol-Related Regulation Genes and PTSD Psychotherapy

Healthcare ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 376
Author(s):  
Ivone Castro-Vale ◽  
Davide Carvalho
Keyword(s):  
Hpa Axis ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Traumatic Event ◽  
Epigenetic Modification ◽  
Pharmacological Treatments ◽  
Post Traumatic Stress ◽  
First Line ◽  
Cardiometabolic Disorders ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) only develops after exposure to a traumatic event in some individuals. PTSD can be chronic and debilitating, and is associated with co-morbidities such as depression, substance use, and cardiometabolic disorders. One of the most important pathophysiological mechanisms underlying the development of PTSD and its subsequent maintenance is a dysfunctional hypothalamic–pituitary–adrenal (HPA) axis. The corticotrophin-releasing hormone, cortisol, glucocorticoid receptor (GR), and their respective genes are some of the mediators of PTSD’s pathophysiology. Several treatments are available, including medication and psychotherapies, although their success rate is limited. Some pharmacological therapies based on the HPA axis are currently being tested in clinical trials and changes in HPA axis biomarkers have been found to occur in response not only to pharmacological treatments, but also to psychotherapy—including the epigenetic modification of the GR gene. Psychotherapies are considered to be the first line treatments for PTSD in some guidelines, even though they are effective for some, but not for all patients with PTSD. This review aims to address how knowledge of the HPA axis-related genetic makeup can inform and predict the outcomes of psychotherapeutic treatments.

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