Serotonergic and Noradrenergic Markers of Post-Traumatic Stress Disorder with and without Major Depression

Maes, Michaël

doi:10.1016/s0893-133x(98)00058-x

Cited by 83 publications

(41 citation statements)

References 56 publications

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“…However, as was suggested earlier, basal levels of NA appear to be normal in PTSD patients and abnormally elevated levels of NA may only occur following stressful stimuli. Maes et al [26] found that PTSD is accompanied by a lower affinity of paroxetine binding sites and that PTSD with concurrent major depression is accompanied by lower affinity · 2 -adrenergic receptors. However, another study suggested that · 2 -adrenergic receptor sensitivity was not altered in PTSD patients [27].…”

Section: Peripheral Evidence Of Noradrenergic Hyperactivity In Ptsd Pmentioning

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: Peripheral Evidence Of Noradrenergic Hyperactivity In Ptsd Pmentioning

confidence: 99%

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

O'Donnell¹,

Hegadoren

Coupland³

2004

Neuropsychobiology

142

106

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“…That finding is in agreement with our results and suggests that cortisol levels are low in comorbid MDE and PTSD as has been shown in PTSD alone. However, not all studies find low cortisol with PTSD alone (Liberzon et al, 1999;Pitman and Orr, 1990;Lemieux and Coe, 1995;Maes et al, 1999;Smith et al, 1989;Baker et al, 1999), perhaps because of subject selection, diagnostic criteria utilized, or other methodological issues. Although hypersuppression in response to dexamethasone has been reported in sexual abuse victims, most of whom had PTSD, compared to normal controls (Stein et al, 1997), normal suppression (Dinan et al, 1990;Halbreich et al, 1989) has also been reported.…”

Section: Hpa Axis Hypoactivity In Ptsd+mdementioning

confidence: 99%

“…A study of the prolactin response to fenfluramine suggests that subjects with PTSD (five of the eight male subjects had comorbid MDE) have a blunted response compared to normal controls (Davis et al, 1999). Some (Fichtner et al, 1995;Maes et al, 1999), but not all (Cicin-Sain et al, 2000;Maguire et al, 1998), reports regarding paroxetine binding to platelets suggest that binding is decreased in PTSD. Lower serotonin in platelet-poor plasma is reported in chronic PTSD although the frequency of comorbidity with MDE is not described (Spivak et al, 1999).…”

Section: Cortisol Response To Serotonin Release By Fenfluramine In MDmentioning

confidence: 99%

Lower Cortisol Levels in Depressed Patients with Comorbid Post-Traumatic Stress Disorder

Oquendo

Echavarría

Galfalvy

et al. 2002

Neuropsychopharmacol

104

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Post-traumatic stress disorder (PTSD) is often comorbid with major depressive episodes (MDEs) and both conditions carry a higher rate of suicidal behavior. Hypothalamic-pituitary-adrenal (HPA) axis and serotonin abnormalities are associated with both conditions and suicidal behavior, but their inter-relation is not known. We determined cortisol response to placebo or fenfluramine in MDE, MDE and PTSD (MDE+PTSD), and healthy volunteers (HVs) and examined the relation of cortisol responses to suicidal behavior. A total of 58 medication-free patients with MDE (13 had MDE+PTSD) and 24 HVs were studied. They received placebo on the first day and fenfluramine on the second day. Cortisol levels were drawn before challenge and for 5 h thereafter. The MDE+PTSD group had the lowest plasma cortisol, the MDE group had the highest, and HVs had intermediate levels. There were no group differences in cortisol response to fenfluramine. Suicidal behavior, sex, and childhood history of abuse were not predictors of baseline or postchallenge plasma cortisol. Cortisol levels increased with age. This study finds elevated cortisol levels in MDE and is the first report of lower cortisol levels in MDE+PTSD. The findings underscore the impact of comorbidity of PTSD with MDE and highlight the importance of considering comorbidity in psychobiology.

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“…Coping with mental stress depends on genetic and exogenous parameters as well as dietary supply of essential micronutrients, such as essential amino acids (7,8,11,35). The two amino acids (L-tryptophan and L-tyrosine), which are precursors of the brain neurotransmitters have been most frequently studied in respect to stress modulation (1,5,8,16,17,25), but the results were inconsistent.…”

mentioning

confidence: 99%

Oral treatment with L-lysine and L-arginine reduces anxiety and basal cortisol levels in healthy humans

et al. 2007

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Dietary supplementation with an essential amino acid L-lysine has been shown to reduce chronic anxiety in humans with low dietary intake of L-lysine. A combination of L-lysine and L-arginine has been documented to normalize hormonal stress responses in humans with high trait anxiety. The present study was carried out in one hundred eight healthy Japanese adults. The aim of study was to find out whether a week-long oral treatment with L-lysine (2.64 g per day) and L-arginine (2.64 g per day) reduces trait and stress-induced state anxiety and basal levels of stress hormones. We confirmed that, without regard to gender, the amino acid treatment significantly reduced both trait anxiety and state anxiety induced by cognitive stress battery. In addition, we found that the treatment with L-lysine and L-arginine decreased the basal levels of salivary cortisol and chromogranin-A (a salivary marker of the sympatho-adrenal system) in male subjects. These results of this double-blind, placebo controlled and randomized study confirm the previous findings in humans and animals and point to a combination of L-lysine and L-arginine as a potentially useful dietary intervention in otherwise healthy humans with high subjective levels of mental stress and anxiety.

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Serotonergic and Noradrenergic Markers of Post-Traumatic Stress Disorder with and without Major Depression

Abstract: Some studies have suggested that disorders in the peripheral and central metabolism of serotonin (5-HT) and noradrenaline (NE) may play roles in the pathophysiology of post-traumatic stress disorder (PTSD

Cited by 83 publications

References 56 publications

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

Lower Cortisol Levels in Depressed Patients with Comorbid Post-Traumatic Stress Disorder

Oral treatment with L-lysine and L-arginine reduces anxiety and basal cortisol levels in healthy humans

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