Neuroendocrine Aspects of PTSD

Yehuda, Rachel

doi:10.1007/3-540-28082-0_13

Cited by 104 publications

(38 citation statements)

References 94 publications

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“…Other studies focusing on chronic stress have also found hypocortisolism in resting conditions and hypersecretion of corticosterone in response to stress in animals [41]. In humans, hypocortisolemia has been associated with periods of prolonged stress [20,21] and atypical depression and PTSD, among other pathologies [8,21,42,43], with excessive cortisol secretion in response to stress in PTSD [42,44]. However, the pathway by which this pattern of altered activity is activated is unclear.…”

Section: Discussionmentioning

confidence: 99%

Coping with Chronic Social Stress in Mice: Hypothalamic-Pituitary-Adrenal/ Sympathetic-Adrenal-Medullary Axis Activity, Behavioral Changes and Effects of Antalarmin Treatment: Implications for the Study of Stress-Related Psychopathologies

Pérez-Tejada¹,

Arregi²,

Gómez-Lázaro³

et al. 2013

Neuroendocrinology

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The aim of this study was to analyze the individual differences that lead to the development of psychopathological changes in response to chronic social stress. We also assessed the ability of an antagonist of the corticotrophin-releasing hormone (CRH) receptors to reverse the effects of stress. Male adult mice were exposed to repeated defeat experiences for 21 days using a sensorial contact model. After 18 days of defeat, two groups of subjects were established (active and passive), according to their behaviors during social confrontation. Antalarmin treatment was given for 4 and 6 days. The results corroborated previous data indicating that subjects who adopted a passive coping strategy had higher corticosterone levels after 21 days of defeat and decreased resting levels 3 days later. Moreover, they showed higher resting expression levels of hypothalamic CRH than their active counterparts. On day 24, the experimental animals were subjected to another social defeat to determine whether the stress response remained. The increase in corticosterone and hypothalamic CRH levels was similar for all of the stressed subjects, but the passive subjects also had a greater CRH response in the amygdala. Passive subjects had decreased levels of adrenal dopamine β-hydroxylase, tyrosine hydroxylase and plasma adrenaline compared to the active subjects, and lower plasma noradrenaline levels than manipulated controls. The passive profile of physiological changes in both the hypothalamic-pituitary-adrenal and sympathetic-adrenal-medullary (SAM) axes has been associated with changes related to mood disorders, such as posttraumatic stress disorder and depression. The active coping profile is characterized by similar corticosterone resting levels to controls and increased SAM activity. Both profiles showed alterations in the novel palatable and forced swimming tests, with the passive profile being the most vulnerable to the effects of stress in this last test. Pharmacological treatment with antalarmin failed to reverse the effects of stress.

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Section: Discussionmentioning

confidence: 99%

Coping with Chronic Social Stress in Mice: Hypothalamic-Pituitary-Adrenal/ Sympathetic-Adrenal-Medullary Axis Activity, Behavioral Changes and Effects of Antalarmin Treatment: Implications for the Study of Stress-Related Psychopathologies

Pérez-Tejada¹,

Arregi²,

Gómez-Lázaro³

et al. 2013

Neuroendocrinology

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“…Cortisol dysregulation and deficient glucocorticoid feedback regulation have been repeatedly identified as biological correlates of adult depression and anxiety disorders [38][39] and early life adversity is consistently associated with these disorders in epidemiological studies. 40 A large body of clinical literature has characterized major depressive disorder (MDD) as a condition associated with excessive basal cortisol secretion and inadequate inhibitory feedback regulation of the HPA axis constituents.…”

mentioning

confidence: 99%

Depressão e estresse: existe um endofenótipo?

Mello

Juruena²,

Pariante³

et al. 2007

Rev. Bras. Psiquiatr.

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A b s t r a c t Objective: To review the new findings about stress, hypothalamic-pituitary-adrenal axis and depression trying to explain a possible endophenotype prone to depression. Method: Nonsystematic review of the literature based on the endophenotype hypothesis. Results: Depression is linked to hypercortisolemia in many patients, but not all patients present these hypothalamicpituitary-adrenal axis dysfunction. The dexamethasone suppression test is not the most accurate test to measure the hypothalamicpituitary-adrenal axis function, and its use in the first studies published probably jeopardized the results. Hypercortisolemia frequently occurs in patients with severe depression, melancholic, either psychotic or nonpsychotic type; it is linked to the presence of a polymorphism in the promoter of the serotonin transporter gene, with a history of childhood abuse or neglect, or other significant stressful experiences like the loss of a parent during childhood and temperament leading to alterations in the response to stress. Conclusions: The alterations of the hypothalamic-pituitary-adrenal axis depend on many factors like severity and type of depression, genotype, history of exposure to stress, temperament, and probably resilience. All these factors together result in an endophenotype thought to be prone to depression.Descriptors: Depression; Corticotropin releasing hormone; Hypothalamus-hypophyseal system; Pituitary-adrenal system; Stress Resumo Objetivo: Revisar os achados recentes sobre a relação entre estresse, eixo hipotálamo-pituitária-adrenal e depressão, na tentativa de explicar um endofenótipo de vulnerabilidade para o desenvolvimento da depressão. Método: Revisão não sistemática da literatura baseada na hipótese de endofenótipo. Resultados: A depressão está relacionada à hipercortisolemia em muitos pacientes; porém, nem todos os deprimidos apresentam esta alteração na função hipotálamo-pituitária-adrenal. Os primeiros estudos publicados observaram esta hiperativação do eixo hipotálamo-pituitária-adrenal por meio do teste de supressão da dexametasona. Estes resultados não foram largamente replicados em grande parte devido à falta de acurária desse teste. A hipercortisolemia ocorre freqüentemente em pacientes com depressão grave, do tipo melancólico, psicóticos ou não. Está relacionada a um polimorfismo específico do gene do transportador da serotonina; a história de abuso ou negligência durante a infância ou perda parental precoce; e ao temperamento que resulta em alterações na resposta ao estresse. Conclusões: As alterações do eixo hipotálamo-pituitária-adrenal dependem de diversos fatores, como gravidade e tipo de depressão, genótipo, história de trauma na infância, temperamento e, provavelmente, resiliência. Todas essas variáveis se relacionam a um endofenótipo vulnerá-vel ao desenvolvimento de depressão.Descritores: Depressão; Fator de liberação de corticotrofina; Sistema hipotálamo hipofisário; Sistema hipófise supra-renal; Estresse

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“…In addition, determining baseline corticosterone levels before and/or after the stress / no stress manipulation would provide for a more comprehensive characterization of the role of the HPA axis in the onset of PTSD-like behaviors. This is important because even after development of the disorder, people with PTSD typically exhibit abnormally low baseline levels of cortisol, a finding that has been speculated to result from enhanced negative feedback of the HPA axis [39][40][41]. Thus, it is not known whether abnormally low cortisol levels are a predisposing, baseline characteristic that enhances these individuals' likelihood of developing PTSD following trauma or if such levels develop as a result of the disorder.…”

Section: Blunted Corticosterone Response To Acute Predator Stress Resmentioning

confidence: 99%

Blunted Corticosterone Response to Acute Predator Stress Results in Long-Term Spatial Memory Impairment

Zoladz

Burke²,

Robinson³

et al. 2014

SOJP

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SOJ Psychology Open Access Research Articlepituitary-adrenal (HPA) axis response to a traumatic event could affect his or her likelihood of developing PTSD [8][9][10]. In these studies, researchers showed that individuals who developed PTSD exhibited significantly lower levels of cortisol after the traumatic event than those individuals who did not develop PTSD. Preclinical work has provided similar results by examining the development of PTSD-like behaviors in different strains of rats. For instance, Cohen and colleagues [11] reported that Lewis rats, which exhibit a significantly blunted corticosterone response to stress, are more prone to developing PTSD-like behaviors following an acute stressor than Fischer or SpragueDawley rats. However, the studies conducted on this topic thus far have not been able to determine whether it is the HPA axis response to an acute stressor that affects PTSD / PTSD-like behavior development or if reduced HPA axis activity is merely a baseline characteristic of the people / rats that are more likely to develop PTSD / PTSD-like behaviors.Only one study of which we are aware has utilized an experimental inhibition of a rat's HPA axis response to stress in order to assess whether or not it would facilitate the development of PTSD-like behaviors. In that study, the investigators found that the combination of a blunted corticosterone and parasympathetic nervous system response to stress resulted in significantly greater anxiety on an elevated plus maze three weeks following a single stress exposure [12]. However, these results were observed when comparing the experimental groups to their respective controls only, and the effects of the manipulations on cognitive performance were not examined. This latter point is especially important because PTSD can be considered a disorder of memory, as individuals suffering from the disorder show marked impairments of learning and memory, a phenomenon that may be a result of intrusive memories transiently interfering with these individuals' ability to process new information [13][14][15][16][17]. Thus, the purpose of the present study was to determine whether or not a blunted HPA axis response to acute predator

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Neuroendocrine Aspects of PTSD

Cited by 104 publications

References 94 publications

Coping with Chronic Social Stress in Mice: Hypothalamic-Pituitary-Adrenal/ Sympathetic-Adrenal-Medullary Axis Activity, Behavioral Changes and Effects of Antalarmin Treatment: Implications for the Study of Stress-Related Psychopathologies

Coping with Chronic Social Stress in Mice: Hypothalamic-Pituitary-Adrenal/ Sympathetic-Adrenal-Medullary Axis Activity, Behavioral Changes and Effects of Antalarmin Treatment: Implications for the Study of Stress-Related Psychopathologies

Depressão e estresse: existe um endofenótipo?

Blunted Corticosterone Response to Acute Predator Stress Results in Long-Term Spatial Memory Impairment

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