Low Plasma β-Endorphin in Post-Traumatic Stress Disorder

Hoffman, L; Watson, Paddy Burges; Wilson, George; Montgomery, Joan

doi:10.3109/00048678909062145

Cited by 61 publications

(26 citation statements)

References 13 publications

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“…Few studies have examined levels of endogenous opioids in PTSD patients. Studies examining ß-endorphin levels have been conflicting with lower [76], comparable [97], and higher levels [98] being reported in PTSD patients compared to controls. In response to exercise-induced stress, PTSD patients were found to have an increased ß-endorphin response in one study [97], while another study found a negative correlation between ß-endorphin levels and avoidant and intrusive symptoms in PTSD patients.…”

Section: Regulation Of the Lc During Stressmentioning

confidence: 99%

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

O'Donnell¹,

Hegadoren

Coupland³

2004

Neuropsychobiology

142

106

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Post-traumatic stress disorder (PTSD) is a serious psychiatric illness that may develop in individuals after exposure to a traumatic event. Recent data suggest that trauma and/or long-term stressors can cause alterations in the functioning of neuroanatomical structures and neural networks throughout the central nervous system. Specifically, dysregulation in central and perhaps, peripheral noradrenergic neural networks has been implicated as the cause of specific symptom clusters in the pathophysiology of PTSD. In this review, both clinical and preclinical data are presented to highlight types of noradrenergic dysfunction observed in individuals with PTSD. Additionally, the role of noradrenaline dysregulation in the acquisition/initiation, and maintenance of hyperarousal and reexperiencing symptom clusters in PTSD will be addressed.

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Section: Regulation Of the Lc During Stressmentioning

confidence: 99%

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

O'Donnell¹,

Hegadoren

Coupland³

2004

Neuropsychobiology

142

106

View full text Add to dashboard Cite

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“…Of particular relevance to the present study, HPA dysregulation has been reported in PTSD, although the exact nature of the dysregulation remains a matter of debate. Some studies have shown elevated basal urinary and plasma cortisol levels in PTSD patients compared to controls (Hoffman et al, 1989;, while others have shown lower urinary and plasma cortisol Yehuda et al, 1990Yehuda et al, , 1993Yehuda et al, , 1995. Again, discrepancies may be related to the nature or duration of the trauma, or to the expression of specific symptoms (de Quervain et al, 2009;Handwerger, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…The mPFC, particularly the infralimbic cortex, is a key region involved in extinction learning (Milad and Quirk, 2002;Quirk et al, 2000;. Furthermore, humans with PTSD display dysregulated hypothalamicepituitaryeadrenal (HPA) axis activity, although the nature of this dysregulation remains unclear Hoffman et al, 1989;Yehuda et al, 1995Yehuda et al, , 1993Yehuda et al, , 1990.…”

Section: Contents Lists Available At Sciverse Sciencedirectmentioning

confidence: 99%

The STRONG STAR Multidisciplinary PTSD Research Consortium

Strong¹,

Frazer²,

Morilak³

2012

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. Email: strong@uthscsa.edu 5f. WORK UNIT NUMBER REPORT DATE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Texas Health Science Center at San Antonio San Antonio, TX 78229 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENT A. INTRODUCTION:Traumatic stress is a requirement for the development of PTSD. However, the majority of trauma-exposed persons do not develop PTSD. Therefore, examination of the typical effects of a stressor may not identify the critical components of PTSD risk or pathogenesis. One obvious explanation for individual differences in vulnerability to PTSD is that there may be genetic predisposition to susceptibility to precipitating stressors. However, to date, very few genetic polymorphisms for PTSD have been identified. An alternative mechanism that would impart lifelong vulnerability to PTSD is stable alterations in gene expression programmed by exposure to early life stressors. Therefore, the hypothesis to be addressed by this project is that early life exposure to stress or glucocorticoids programs a distinct neurochemical and behavioral phenotype during adulthood characterized by vulnerability to stressors that trigger PTSD. Moreover, we hypothesize that the susceptibility to PTSD can be reversed in adult offspring by anti-depressants that have been reported to reverse the epigenetic changes in expression of selected genes caused by stress. To address this hypothesis, we proposed the following specific aims: 1. To generate and characterize models of early life stress: prenatal stress; prenatal glucocorticoid receptor stimulation; and perinatal stress and perinatal glucocorticoid exposure. 2.To determine adult predictors of vulnerability to stress: as determined by behavioral, physiological, and molecular and neurochemical measures. 3. To determine adult vulnerability to stress: Adult offspring from models developed in Specific Aim 1 are exposed to a ...

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“…For these reasons, the relations of beta-endorphin with traumas and related disorders are also examined, post-traumatic stress disorder (PTSD) among them (Merenlender-Wagner et al, 2009). Hoffman et al (1989) propose plasma β-endorphin as a marker for PTSD after finding the hormone diurnal levels to be significantly lower than in controls. Although traumas are not explicitly included in the diagnosis of any type of depression as they are in PTSD, trauma history is a factor in etiology of depression.…”

Section: Introductionmentioning

confidence: 95%