Hypodensity of platelet serotonin uptake sites in posttraumatic stress disorder: Associated clinical features

Fichtner, Christopher G.; O'Connor, Francine L.; Yeoh, H.C.; Arora, Ramesh; Crayton, John W.

doi:10.1016/0024-3205(95)00262-5

Cited by 26 publications

(12 citation statements)

References 52 publications

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“…No change ([ 14 C]serotonin uptake) [234] Decrease (human platelets, [ 3 H]paroxetine binding) [323,324] Social phobia Platelet studies:…”

Section: Polymorphism Studiesmentioning

confidence: 99%

Neuroimaging of the Serotonin Transporter: Possibilities and Pitfalls

Brust¹,

Hesse²,

Müller³

et al. 2006

CPSR

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Nuclear medicine imaging techniques like positron emission tomography (PET) and single-photon emission computed tomography (SPECT) apply radiolabeled drugs that bind selectively to specific neurotransmitter receptors and transporters such as the serotonin transporter (SERT) in the living human brain. They can help overcome certain limitations of postmortem, platelet and genetic studies of the SERT. This review compares the outcome of those studies with recent neuroimaging findings. The first part of this review deals with the choice of radioligands used to quantify SERT distribution in the human brain. The second part summarizes studies performed to understand the normal physiology of the serotonergic system. Selective serotonin reuptake inhibitors (SSRIs), used to treat a wide range of neuropsychiatric disorders with emotional instability and behavioral control deficits, compete with SERT radioligands and have been investigated in pharmacological PET and SPECT studies in healthy volunteers and patients. Part three reviews SERT imaging studies in patients, which have meanwhile been performed in most disorders that benefit from SSRI treatment. It is hypothesized that serotonin deficits and neuropsychiatric symptoms are linked by the inhibition of involuntary emotional reactions to external and internal stimuli. This could explain, why the consistency of many SERT neuroimaging findings is low, and may help develop individual treatment strategies in therapy-nonresponsive cases and to engineer new drugs for the therapy of neuropsychiatric disorders.

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“…No change ([ 14 C]serotonin uptake) [234] Decrease (human platelets, [ 3 H]paroxetine binding) [323,324] Social phobia Platelet studies:…”

Section: Polymorphism Studiesmentioning

confidence: 99%

Neuroimaging of the Serotonin Transporter: Possibilities and Pitfalls

Brust¹,

Hesse²,

Müller³

et al. 2006

CPSR

View full text Add to dashboard Cite

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“…Alternatively, a traumatic experience such as sexual abuse may result in psychobiological dysregulation, which may negatively influence maladaptive behaviours, including disordered eating (23,36). CSA or similar traumas may cause disturbances in the 5‐hydroxytryptamine [5‐HT] pathway (37–39), which has been shown to play a key role in the regulation of eating behaviour (40–42). The role of 5‐HT in the development of obesity, however, awaits further study.…”

Section: Possible Explanations Of the Csa–obesity Relationshipmentioning

confidence: 99%

Childhood sexual abuse and obesity

2004

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SummaryThe causes of the current obesity epidemic are multifactorial and include genetic, environmental, and individual factors. One potential risk factor may be the experience of childhood sexual abuse. Childhood sexual abuse is remarkably common and is thought to affect up to one-third of women and one-eighth of men. A history of childhood sexual abuse is associated with numerous psychological sequelae including depression, anxiety, substance abuse, somatization, and eating disorders. Relatively few studies have examined the relationship between childhood sexual abuse and adult obesity. These studies suggest at least a modest relationship between the two. Potential explanations for the relationship have focused on the role of disordered eating, particularly binge eating, as well as the possible 'adaptive function' of obesity in childhood sexual abuse survivors. Nevertheless, additional research on the relationship between childhood sexual abuse and obesity is clearly needed, not only to address the outstanding empirical issues but also to guide clinical care.

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“…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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Hypodensity of platelet serotonin uptake sites in posttraumatic stress disorder: Associated clinical features

Cited by 26 publications

References 52 publications

Neuroimaging of the Serotonin Transporter: Possibilities and Pitfalls

Neuroimaging of the Serotonin Transporter: Possibilities and Pitfalls

Childhood sexual abuse and obesity

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

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