Paroxetine binding in the blood platelets of post-traumatic stress disorder patients

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

doi:10.1016/0024-3205(93)90444-8

Cited by 64 publications

(27 citation statements)

References 45 publications

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“…The significant and positive correlations between severity of PTSD, either the avoidancedepression or arousal-anxiety symptoms, may suggest that graded differences in the expression of PTSD symptoms are related to changes in the 5-HT transporter system. Arora et al (1993) (Galzin et al 1988;Lawrence et al 1990;D'Hondt et al 1994). These negative findings in major depression are in agreement with our results that there were no significant differences in platelet [ A question, however, is whether peripheral findings are relevant for central serotonergic activity.…”

Section: Discussionsupporting

confidence: 88%

“…First, selective 5-HT reuptake inhibitors (SSRIs), such as fluoxetine, have beneficial effects in the treatment of PTSD (van der Kolk et al 1994). Second, platelet [ 3 H]-paroxetine binding B max and Kd values were significantly lower in PTSD patients than in normal controls, suggesting a lower number of platelet 5-HT transporters in PTSD patients (Arora et al 1993). The 5-HT transporter plays a critical role in 5-HT neurotransmission by reclaiming synaptic 5-HT.…”

Section: Some Studies Have Suggested That Disorders In the Peripheralmentioning

confidence: 99%

“…The 5-HT transporter plays a critical role in 5-HT neurotransmission by reclaiming synaptic 5-HT. Arora et al (1993) (Fichtner et al 1994). However, whether PTSD is accompanied by lower availability of plasma total tryptophan, the precursor of 5-HT, remains elusive.…”

Section: Some Studies Have Suggested That Disorders In the Peripheralmentioning

confidence: 99%

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

Maes

1999

Neuropsychopharmacology

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Section: Discussionsupporting

confidence: 88%

Section: Some Studies Have Suggested That Disorders In the Peripheralmentioning

confidence: 99%

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

Maes

1999

Neuropsychopharmacology

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“…49,50 PTSD has been associated with alterations in platelet serotonin receptor binding. [51][52][53][54][55][56][57][58][59][60][61][62] Serotonin has been shown to enhance glucocorticoid signaling, 63 and increase the number and functional capacity of corticoid receptors in the hippocampus, 64,65 which may influence glucocorticoid responsiveness. 66 Recently, increased glucocorticoid sensitivity was found to be associated with hypocortisolism, reflected by the absence of cortisol response after awakening and lower daytime cortisol levels in Bosnian war refugees with PTSD.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Stress Reactivity After Long‐Term Treatment with Paroxetine in Women with Posttraumatic Stress Disorder

Vermetten

Vythilingam

Schmahl

et al. 2006

Annals of the New York Academy of Sciences

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Posttraumatic stress disorder (PTSD) is typically accompanied by both acute and chronic alterations in the stress response. These alterations have mostly been described in individuals under baseline conditions, but studies have also used a challenge model to assess the role of the hypothalamic-pituitary-adrenal (HPA) axis in the stress response. The purpose of this article was to assess the effect of long-term treatment with the selective reuptake inhibitor (SSRI), paroxetine, on stress reactivity in patients with PTSD. We assessed diurnal salivary cortisol and urinary cortisol as well as cortisol, heart rate, and behavioral responses to a standardized cognitive stress challenge, in 13 female patients with chronic PTSD before and after 12 months of paroxetine treatment. Treatment resulted in a significant decrease in PTSD symptoms. Twenty-four-hour urinary cortisol was lower compared to base line after successful treatment. Treatment resulted in a decrease of salivary cortisol levels on all time points on a diurnal curve. Despite similar stress perception, cortisol response to the cognitive stress challenge resulted in a 26.5% relative decrease in stress-induced salivary cortisol with treatment. These results suggest that successful treatment with SSRI in chronic PTSD is associated with a trend for a decrease in baseline diurnal cortisol and with reduced cortisol reactivity to stress.

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“…Alterations in dopamine (Yehuda et al 1992), norepinephrine (NE) (Geracioti et al 2001), and serotonin (5-HT) (Arora et al 1993) transmission are thought to contribute to the symptoms commonly observed in PTSD patients, including hypervigilance, impulsivity, exaggerated startle, and depressed mood, and may be subject to epigenetic regulation. For example, levels of the enzymes tyrosine hydroxylase (TH) and tryptophan hydroxylase (TPH), responsible for creating precursor metabolites for the production of dopamine (DA), epinephrine, NE, and 5-HT, were found to be significantly decreased in the hippocampus of chronically stressed rats , concurrent with decreased hippocampal acetylation of H3K9 and H4K12 and increased levels of HDAC5.…”

Section: Stress-related Epigenetic Modification Of Stress-related Neumentioning

confidence: 99%

Epigenetic programming of the neuroendocrine stress response by adult life stress

Dirven

Homberg

Kozicz

et al. 2017

Journal of Molecular Endocrinology

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The hypothalamic-pituitary-adrenal (HPA) axis is critically involved in the neuroendocrine regulation of stress adaptation, and the restoration of homeostasis following stress exposure. Dysregulation of this axis is associated with stress-related pathologies like major depressive disorder, post-traumatic stress disorder, panic disorder and chronic anxiety. It has long been understood that stress during early life can have a significant lasting influence on the development of the neuroendocrine system and its neural regulators, partially by modifying epigenetic regulation of gene expression, with implications for health and well-being in later life. Evidence is accumulating that epigenetic plasticity also extends to adulthood, proposing it as a mechanism by which psychological trauma later in life can long-lastingly affect HPA axis function, brain plasticity, neuronal function and behavioural adaptation to neuropsychological stress. Further corroborating this claim is the phenomenon that these epigenetic changes correlate with the behavioural consequences of trauma exposure. Thereby, epigenetic modifications provide a putative molecular mechanism by which the behavioural phenotype and transcriptional/translational potential of genes involved in HPA axis regulation can change drastically in response to environmental challenges, and appear an important target for treatment of stress-related disorders. However, improved insight is required to increase their therapeutic (drug) potential. Here, we provide an overview of the growing body of literature describing the epigenetic modulation of the (primarily neuroendocrine) stress response as a consequence of adult life stress and interpret the implications for, and the challenges involved in applying this knowledge to, the identification and treatment of stress-related psychiatric disorders.

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Paroxetine binding in the blood platelets of post-traumatic stress disorder patients

Cited by 64 publications

References 45 publications

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

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

Alterations in Stress Reactivity After Long‐Term Treatment with Paroxetine in Women with Posttraumatic Stress Disorder

Epigenetic programming of the neuroendocrine stress response by adult life stress

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