Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have reported hyperactivation of catecholaminergic systems and elevated concentrations of corticotropin-releasing-hormone (CRH) in the cerebrospinal fluid (CSF) of child maltreatment victims or combat veterans with post-traumatic stress disorder (PTSD). This study investigated the CSF concentrations of CRH and monoamine metabolites in rhesus macaque mothers that physically abused their infants and had themselves been abused as infants. Ten abusive mothers and 10 controls served as study subjects. All animals were sampled for CSF during pregnancy and the postpartum period. Focal observations of social and maternal behavior were also made. Abusive mothers had significantly higher CSF concentrations of CRH and 5-HIAA than controls. Across both subjects and controls, higher CRH, 5-HIAA and MHPG concentrations were associated with anti-social behavior patterns including a high frequency of maternal aggression, infant rejection, and a low frequency of contacts received from other individuals. These findings are consistent with those of previous primate and human studies and suggest that the neurobiological alterations associated with infant abuse may play an important role in the occurrence of maladaptive behavior in adulthood, including the perpetuation of infant abuse across generations.
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PMID:Neurobiological characteristics of rhesus macaque abusive mothers and their relation to social and maternal behavior. 1565 54

Evidence suggests that individuals with posttraumatic stress disorder (PTSD) have enhanced sensitization of the hypothalamic-pituitary-adrenocortical (HPA) axis. Fourteen adolescent inpatients with DSM-IV PTSD were compared with 14 adolescent hospitalized controls without current axis I diagnoses. All patients were drug-naive. The causative trauma had been sexual abuse in all cases. Dexamethasone, 1 mg orally, was given at 11 PM, 5 days after admission. Baseline blood samples were obtained at 8 AM, and on the following day, adrenocorticotropin (ACTH) and cortisol levels were measured at 8 AM, 4 PM, and 11 PM. Clinical assessment included the Impact of Event Scale, Stanford Acute Stress Reaction Questionnaire, Beck Depression Inventory, and Coping Inventory for Stressful Situations. Post-DST ACTH levels were significantly lower in PTSD than in control adolescents (at 8 AM, P <0.005; at 4 PM, P <0.001; and at 11 PM, P <0.05). In patients, post-DST cortisol levels were reduced but not significantly. No correlations were found between ACTH and cortisol levels and time elapsed since trauma. These results demonstrate that sexually abused adolescents with PTSD show ACTH hypersuppression to DST, suggesting enhanced glucocorticoid receptor sensitivity in the pituitary.
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PMID:Increased adrenocorticotropin suppression after dexamethasone administration in sexually abused adolescents with posttraumatic stress disorder. 1567 26

The authors examined the Trauma Symptom Inventory's (TSI) ability to discriminate 88 student post-traumatic stress disorder (PTSD) simulators screened for genuine PTSD from 48 clinical PTSD-diagnosed outpatients. Results demonstrated between-group differences on several TSI clinical scales and the Atypical Response (ATR) validity scale. Discriminant function analysis using ATR revealed 75% correct patient classification but only 48% correct simulator classification, with an overall correct classification rate of 59% (positive predictive power [PPP] = .71; negative predictive power [NPP] = .51). Individual ATR cutoff scores did not yield impressive classification results, with the optimal cutoff (T score = 61) correctly classifying only 61% of simulators and patients (PPP = .66, NPP = .54). Although ATR was not developed as a malingered PTSD screen, instead serving as a general validity screen, caution is recommended in its current clinical use for detecting malingered PTSD.
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PMID:Utility of the trauma symptom inventory's atypical response scale in detecting malingered post-traumatic stress disorder. 1591 22

The key neuroendocrine component of a response to stress is the hypothalamic-pituitary-adrenocortical (HPA) system. Abnormalities in the HPA system have been implicated in the pathophysiology of psychiatric disorders such as depression, post-traumatic stress disorder, alcoholism and suicide. The dexamethasone suppression test (DST) is the most frequently used test to assess HPA-system function in psychiatric disorders. This neuroendocrine test consists of the administration of a low dose of dexamethasone at 11 pm and the measurement of cortisol levels at one or more time points on the following day. After corticotropin-releasing hormone (CRH) became available for clinical studies, the DST was combined with CRH administration. In this test, patients are pretreated with a single dose of dexamethasone at 11 pm and receive human CRH intravenously at 3 pm the following day. The resulting DST-CRH test proved to be much more sensitive in detecting HPA system alterations than the DST. We have modified the DST-CRH test and used ovine CRH instead of human CRH in a pilot study of a group of young healthy volunteers. Results indicated that it produces results similar to the results obtained with human CRH. This suggests that ovine CRH can be used in psychiatric research. Alcoholism is associated with abnormalities in HPA function. Nonalcoholic subjects with a family history of alcoholism exhibit lower plasma ACTH and beta-endorphin as well as lower ACTH, cortisol, and beta-endorphin responses to psychological stress and CRH stimulation. This suggests that in children of alcoholics, alterations in the mechanisms that regulate HPA axis activity predate the development of alcohol dependence and may be considered inherited traits. Therefore, studies of the HPA system in persons at risk for alcoholism may help understand the neurobiological mechanisms of predisposition to alcoholism.
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PMID:Modified dexamethasone suppression-corticotropin-releasing hormone stimulation test: A pilot study of young healthy volunteers and implications for alcoholism research in adolescents and young adults. 1663 67

In humans changes in serum cortisol levels have been observed with aging, stress, and with affective disorders such as major depression and post-traumatic stress disorder. Corticosteroids are known to influence hippocampal structure and function; specifically, plasma corticosteroid levels have been inversely correlated with hippocampal cell proliferation, cell death, and impaired memory function. The relationship between corticosteroids and structure and function of the hippocampus has been studied in experimental systems in adult animals by increasing or decreasing corticosterone levels through pharmacological supplementation and through surgical removal of the adrenal gland. Here, we utilized the genetically engineered pro-opiomelanocortin (POMC) null mutant mouse, which because of the lack of all POMC peptides has no corticosterone from birth throughout life. The effect of this lifelong absence of corticosterone on the dentate gyrus of the hippocampus is a decrease in granule cell density, which correlated with a decrease in cell proliferation but not an increase in cell degeneration. Fine morphology of granule cells was unaltered. Analyses of gene expression revealed no changes in POMC null mutant vs wild-type hippocampus with respect to levels of expression of corticoid receptor genes or genes known to be regulated by corticosterone. Spatial learning as tested by the Morris water maze was not altered in the POMC null mutant mouse. Taken together with findings from other studies of the effects of altered levels of corticosteroids on the hippocampus, our results argue for a complex homeostasis in which disturbances of any one factor can offset the system in varying ways.
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PMID:Effects on hippocampus of lifelong absence of glucocorticoids in the pro-opiomelanocortin null mutant mouse reveal complex relationship between glucocorticoids and hippocampal structure and function. 1669 Oct 17

The basis of postdeployment health symptoms in Gulf War veterans remains poorly understood. Alterations in the feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis have been demonstrated in posttraumatic stress disorder (PTSD) and other bodily disorders related to stress. The objective of this article was to examine whether similar HPA axis alterations are related to Gulf War deployment, postdeployment health symptoms, or PTSD. Plasma adrenocorticotropic hormone (ACTH) was measured on consecutive mornings at 08:00 h before and after a low dose of oral dexamethasone (DEX) at 23:00 h in Gulf War veterans with PTSD (n = 14), Gulf War veterans without PTSD (n = 11), and healthy veterans never deployed to a war zone (n = 12). Both Gulf War veterans with PTSD and Gulf War veterans without PTSD had significantly lower post-DEX ACTH levels than the nonexposed veterans, in the absence of group differences in basal ACTH or DEX levels. Among Gulf War veterans, post-DEX ACTH levels were significantly associated with musculoskeletal symptoms. Gulf War deployment and postdeployment health symptoms appear to be associated with alterations in feedback regulation of the pituitary gland that suggests a possible common link between postdeployment health symptoms and other chronic stress-related conditions.
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PMID:The ACTH response to dexamethasone in Persian Gulf War veterans. 1689 96

The stress response alters behavior, autonomic function, and secretion of multiple hormones, including corticotropin-releasing factor, adrenocorticotropin hormone, and cortisol, through the hypothalamic-pituitary-adrenal axis. Constitutive stress responses lead to a number of psychiatric disorders, including depression, posttraumatic stress disorder, Alzheimer's disease (AD), and other anxiety disorders through increased stress hormones and other unknown factors. Here, we performed a proteomic analysis of rat brain exposed to restraint stress compared with a nonstress group by using 2D-DIGE and MALDI-TOF analysis. Several proteins were identified by peptide mass fingerprint (PMF), including down-regulated hippocampal cholinergic neurostimulating peptide precursor protein (HCNP-pp). The current study demonstrates that HCNP-pp mRNA and protein expression are decreased in rat hippocampus after stress exposure. The level of HCNP-pp in H19-7, a rat hippocampal cell line, significantly decreases with dexamethasone treatment, a synthetic glucocorticoid. Thus, this finding suggests that HCNP-pp expression may decrease in response to stress exposure. Decreased HCNP-pp from stress exposure may result in lower levels of HCNP that might contribute to a loss of acetylcholine production.
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PMID:Decreased hippocampal cholinergic neurostimulating peptide precursor protein associated with stress exposure in rat brain by proteomic analysis. 1762 2

Survivors of the acute respiratory distress syndrome (ARDS) often report traumatic memories from the intensive care unit (ICU) and display a high incidence of post-traumatic stress disorder (PTSD). As it is known that subjects with PTSD often show sustained reductions in circulating cortisol concentrations, we examined the relationship between serum cortisol, traumatic memories and PTSD in patients after ARDS. We evaluated 33 long-term survivors of ARDS (7.5+/-2.9 years after discharge from the ICU) for pre-defined categories of traumatic memory from the ICU, hypothalamic-pituitary-adrenocortical axis reactivity to corticotropin and PTSD (by psychiatric interview). During evaluation, patients with multiple traumatic memories had significantly lower basal serum cortisol levels when compared to patients with no or only 1 category of traumatic memory, with no differences in peak cortisol levels after corticotropin stimulation between both subgroups. There was a significant negative correlation between basal cortisol levels and the number of traumatic memories present. PTSD symptom scores correlated with the number of traumatic memories but not with cortisol levels. These findings indicate that lower baseline cortisol levels in long-term survivors of ARDS are associated with an increased incidence of traumatic memories from the ICU, and that more traumatic memories are related to a higher incidence and intensity of PTSD symptoms.
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PMID:Traumatic memories, post-traumatic stress disorder and serum cortisol levels in long-term survivors of the acute respiratory distress syndrome. 1937 97

Long known for its anti-nociceptive effects, the opioid beta-endorphin is also reported to have rewarding and reinforcing properties and to be involved in stress response. In this manuscript we summarize the present neurobiological and behavioral evidence regarding the role of beta-endorphin in stress-related psychiatric disorders, depression and PTSD. There is existing data that support the importance of beta-endorphin neurotransmission in mediating depression. As for PTSD, however, the data is thus far circumstantial. The studies described herein used diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and behavioral monitoring, in two animal models of depression and PTSD. We suggest that the pathways for stress-related psychiatric disorders, depression and PTSD, converge to a common pathway in which beta-endorphin is a modulating element of distress. This may occur via its interaction with the mesolimbic monoaminergic system and also by its interesting effects on learning and memory. The possible involvement of beta-endorphin in the process of stress-related psychiatric disorders, depression and PTSD, is discussed.
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PMID:The beta-endorphin role in stress-related psychiatric disorders. 1970 53

Current findings about dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulphate (DHEA-S) in patients with post-traumatic stress disorder (PTSD) have been inconsistent. We investigated whether a history of severe childhood traumatisation affects these steroids in PTSD patients. Patients of 33 with chronic PTSD (15 with and 18 without sexual and/or severe physical abuse before age 12) were studied in a combined low dose dexamethasone/corticotropin-releasing hormone (CRH) test. Mean pre-CRH levels of both plasma DHEA and DHEA-S were significantly increased in the subgroup with childhood abuse, the respective ratios with plasma cortisol were significantly lower. In the entire population of PTSD patients significant amounts of the variation of these parameters could be explained by childhood trauma history. Further studies are needed to clarify the potential role of DHEA and DHEA-S as biomarkers for severe early adverse events in patients suffering from PTSD and in other stress-related disorders.
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PMID:Increased DHEA and DHEA-S plasma levels in patients with post-traumatic stress disorder and a history of childhood abuse. 1975 39


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