Elevated circulatory level of GABA<sub>A</sub> – antagonistic neurosteroids in 
patients with combat-related post-traumatic stress disorder

Spivak, Baruch; Maayan, Rachel; Kotler, Moshe; Mester, Roberto; Gil-Ad, Irit; Shtaif, Biana; Weizman, Abraham

doi:10.1017/s0033291799002731

Cited by 124 publications

(74 citation statements)

References 22 publications

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“…Studies of DHEA in patients with stressrelated psychiatric disorders are contradictory, while studies in adult depressed patients showed both increases (Heuser et al, 1998) and decreases as well as no change (Michael et al, 2000;Young et al, 2002) in levels. Studies of DHEA in PTSD have been equally contradictory, with one study citing lower concentrations relative to controls (Kanter et al, 2001) while the other showed elevations (Spivak et al, 2000). We recently measured DHEA and DHEA-S at multiple time points over a 24 h period in women with early abuse and PTSD, and found elevations in both DHEA and DHEA-S (Bremner et al, 2007).…”

Section: Stress and Neurohormonal Systemsmentioning

confidence: 99%

Structural and functional plasticity of the human brain in posttraumatic stress disorder

Bremner

Elzinga

Schmahl

et al. 2007

Progress in Brain Research

286

186

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Posttraumatic stress disorder (PTSD) is associated with long-term changes in neurobiology. Brain areas involved in the stress response include the medial prefrontal cortex, hippocampus, and amygdala. Neurohormonal systems that act on the brain areas to modulate PTSD symptoms and memory include glucocorticoids and norepinephrine. Dysfunction of these brain areas is responsible for the symptoms of PTSD. Brain imaging studies show that PTSD patients have increased amygdala reactivity during fear acquisition. Other studies show smaller hippocampal volume. A failure of medial prefrontal/anterior cingulate activation with re-experiencing of the trauma is hypothesized to represent a neural correlate of the failure of extinction seen in PTSD. The brain has the capacity for plasticity in the aftermath of traumatic stress. Antidepressant treatments and changes in environment can reverse the effects of stress on hippocampal neurogenesis, and humans with PTSD showed increased hippocampal volume with both paroxetine and phenytoin.

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Section: Stress and Neurohormonal Systemsmentioning

confidence: 99%

Structural and functional plasticity of the human brain in posttraumatic stress disorder

Bremner

Elzinga

Schmahl

et al. 2007

Progress in Brain Research

286

186

View full text Add to dashboard Cite

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“…DHEA is known to have neuroprotective and functionally enhancing properties in animal studies [49] and has been linked with resilience-related qualities such as self-efficacy, optimism, social support and well-being in a non-clinical sample [50]. We and others have reported increased DHEA and DHEA-S in association with recovery from PTSD in combat veterans [38,51], a finding that has also been observed in civilian trauma survivors with PTSD [14]. More recently, DHEA was demonstrated to have anabolic properties, whereas DHEA-S has been shown to have neuroprotective qualities in warfighters, a fact that has led to treatment trials with DHEA and DHEA-S supplementation during military training [48,52].…”

Section: Resilience-related Prognostic Markersmentioning

confidence: 72%

Glucocorticoid-related predictors and correlates of post-traumatic stress disorder treatment response in combat veterans

et al. 2014

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One contribution of 9 to a Theme Issue 'Towards a systems model of resilience'. The identification of biomarkers for post-traumatic stress disorder (PTSD) and resilience/recovery is critical for advancing knowledge about pathophysiology and treatment in trauma-exposed persons. This study examined a series of glucocorticoid-related biomarkers prior to and in response to psychotherapy. Fifty-two male and female veterans with PTSD were randomized 2 : 1 to receive either prolonged exposure (PE) therapy or a weekly minimal attention (MA) intervention for 12 consecutive weeks. Psychological and biological assessments were obtained prior to and following treatment and after a 12-week naturalistic follow-up. Response was defined dichotomously as no longer meeting criteria for PTSD at post-treatment based on the Clinician Administered PTSD Scale for DSM-IV (CAPS). Clinical improvement on the CAPS was apparent for both PE and MA, with no significant difference according to treatment condition. Biomarkers predictive of treatment gains included the BCLI polymorphism of the glucocorticoid receptor gene. Additional predictors of treatment response were higher bedtime salivary cortisol and 24 h urinary cortisol excretion. Pre-treatment plasma dehydroepiandrosterone/ cortisol ratio and neuropetide Y (NPY) levels were predictors of reductions in PTSD symptoms, and, for NPY only, of other secondary outcomes as well, including anxiety and depression ratings. Glucocorticoid sensitivity changed in association with symptom change, reflecting clinical state. It is possible to distinguish prognostic and state biomarkers of PTSD using a longitudinal approach in the context of treatment. Identified markers may also be relevant to understanding mechanisms of action of symptom reduction.

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“…Furthermore, several studies have pointed out that 17-α-OH-P affects some neurological functions; through the activation of GABA A receptor, which exert an inhibitory function on the SNC 46) . Progesterone and its metabolites can induce psychological disorders in men, such as panic attacks 49) , mood disorders (depression and post-traumatic stress disorders) 50) and anxiety 51) . High levels of 17-α-OH-P have also been reported in schizophrenic men 52) .…”

Section: Discussionmentioning

confidence: 99%

“…17-α-O H -P h a s d i r e c t e ff e c t s u p o n t h e p r o c e s s o f spermatogenesis [42][43][44][45] and on the Central Neural System (SNC) where it acts as a positive or a negative modulator of GABA A receptor (γ-amminobutirric-acid A ) 46) ; moreover, it regulates several activities, such as learning, memory 47) and sleep 48) . Furthermore, according to other studies alterations in plasma 17-α-OH-P levels could cause mental health disorders in male subjects, for instance: panic attacks, anxiety, post traumatic stress disorders, depression and schizophrenia [49][50][51][52] . The aim of the study is to evaluate if the occupational exposure to urban pollutants could cause alterations on 17-α-OH-P plasma levels and related diseases in traffic policemen compared to a control group.…”

Section: Introductionmentioning

confidence: 86%

Plasma 17-α-OH-progesterone in Male Workers Exposed to Traffic Pollutants

et al. 2007

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The aim of the study is to evaluate if the occupational exposure to urban pollutants could cause alterations on 17-alfa-hydroxy-progesterone plasma levels and related diseases in male traffic policemen. 17-α α α α α-OH-P is synthesized in Leydig cells and in adrenals; it influences spermiogenesis, acrosoma reaction, testosterone biosynthesis, blocking of gonadotropin secretion; it regulates learning, memory and sleep. After excluding principal confounding factors, i.e., rotating or night shifts, exposure to solvents, paints and pesticides during time-off and smoking, traffic policemen were matched with controls by age, working life and drinking habit. Finally, 112 traffic policemen and 112 controls were included in the study. In traffic policemen 17-α α α α α-OH-P mean values were significantly higher vs. controls. The distribution of 17-α α α α α-OH-P values in both groups was significant. An increased frequency of fertility disorders referred to the questionnaire items were found in traffic policemen vs. controls, but the difference was not significant. The occupational exposure to low doses of chemical urban stressor, interacting with and adding to the psychosocial ones, could alter plasma 17-α α α α α-OH-P concentrations in traffic policemen vs. controls. 17-α α α α α-OH-P could be used as an early biological marker, even before the onset of the reproductive and mental health diseases.

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Elevated circulatory level of GABA_A – antagonistic neurosteroids in patients with combat-related post-traumatic stress disorder

Cited by 124 publications

References 22 publications

Structural and functional plasticity of the human brain in posttraumatic stress disorder

Structural and functional plasticity of the human brain in posttraumatic stress disorder

Glucocorticoid-related predictors and correlates of post-traumatic stress disorder treatment response in combat veterans

Plasma 17-α-OH-progesterone in Male Workers Exposed to Traffic Pollutants

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Elevated circulatory level of GABAA – antagonistic neurosteroids in patients with combat-related post-traumatic stress disorder

Cited by 124 publications

References 22 publications

Structural and functional plasticity of the human brain in posttraumatic stress disorder

Structural and functional plasticity of the human brain in posttraumatic stress disorder

Glucocorticoid-related predictors and correlates of post-traumatic stress disorder treatment response in combat veterans

Plasma 17-α-OH-progesterone in Male Workers Exposed to Traffic Pollutants

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Elevated circulatory level of GABA_A – antagonistic neurosteroids in patients with combat-related post-traumatic stress disorder