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)

The endogenous morphinomimetic brain peptides Met5-enkephalin and alpha-, beta-, and gamma-endorphins have been evaluated in rats after intracerebrospinal fluid injection. beta-Endorphin produces marked, prolonged muscular rigidity and immobility similar to a catatonic state, counteracted by the opiate antagonist naloxone; this effect occurs at molar doses 1/100 to 1/400 that at which the other peptides or morphine block the response to painful stimuli. All peptides evoked dose-related, naloxone-reversible, wet-dog shakes in rats that had not been exposed to drugs. beta-Endorphin produced hypothermia, whereas gamma-endorphin produced hyperthermia. Such potent and divergent responses to naturally occurring subtances suggest that alterations in their homeostatic regulation could have etiological significance in mental illness.
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PMID:Endorphins: profound behavioral effects in rats suggest new etiological factors in mental illness. 18 94

In this study we assessed the role of psychological factor in the etiology of coronary vasospasm using the Cornell Medical Index (CMI), focusing attention on the relationship between stress and serum magnesium (Mg). The study subjects consisted of 25 patients with variant angina (VA), 32 with old myocardial infarction without vasospasm (OMI), and 34 healthy men (controls). On a neurosis-discriminative diagram of CMI, areas I and II were considered as normal and areas III and IV were considered to be a neurotic disorder. The stress test included exercise and a quiz. Exercise test was performed in 8 patients with VA, 6 with OMI, and 5 controls, and a quiz was given to 4 patients with VA. Plasma catecholamines [noradrenaline (NA), adrenaline (Ad), dopamine], aldosterone, adrenocorticotropic hormone (ACTH) and serum electrolytes (Mg, Ca, Na, K, Cl) were measured before and after exposures to stress. The following results were obtained: 1) Of the patients with VA, 40.0% were categorized as area III or IV, compared to 18.7% of the patients with OMI, and 2.9% of the control subjects. 2) Among patients with VA, 64.0% exhibited anxiety states compatible with a psychological disorder. 3) NA and Ad were increased after exercise stress. 4) Serum Mg and Ca were also increased after exposure to exercise stress in all groups, and the degrees of these changes were correlated to the exercise intensity. The %delta Mg/%delta NA ratio, a parameter of the effect of catecholamine on the serum Mg, was greater in patients with VA than in those with OMI and the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The relation of physical and mental stress to magnesium deficiency in patients with variant angina]. 133 93

This article presents a series of experiments that involves the development of three novel strategies for human stress research and the utilization of these strategies to examine neurobehavioral processes of stress in healthy volunteers, schizophrenia, and affective illness. The first strategy involved intravenous 2-deoxy-D-glucose (2DG) administration, a glucoprivic stressor. We found that glucoprivic stress results in dissociation of hypothalamus-pituitary-adrenal (HPA), adrenomedullary, and sympathoneural activity. In addition, glucoprivic stress in neuroleptic-treated schizophrenic patients caused heightened dopamine activity, as reflected by increased plasma homovanillic acid (HVA) levels and decreased adaptive responses as assessed by decreased food consumption following 2DG administration. These data suggest that neuroleptics do not prevent stress-related increases in dopamine activity and that schizophrenia may be associated with abnormalities in the stress response. The second strategy assessed effects of uncontrollable and identical amounts of controllable stress in volunteers and depressed patients. In volunteers, it was found that uncontrollable in comparison to controllable stress results in specific behavioral and neuroendocrine alterations. Moreover, uncontrollable stress exposure in depressed patients in comparison to volunteers produced greater alterations in behavioral ratings and plasma cortisol levels and that the uncontrollable stress related increases in helplessness ratings and cortisol levels were significantly correlated. These data suggest that depressed patients may have increased sensitivity to uncontrollable stress and that there may be an important interrelationship between the cognitive deficits of depression and the heightened HPA axis activity observed in these patients. Lastly, we used a naturalistic strategy to examine mechanisms relating childhood parental loss and the development of adult affective illness and found that among subjects with early parental loss histories, those who developed adult psychiatric illness had increased resting plasma levels of cortisol and beta-endorphin (ir) as compared with subjects with early loss and no adult history of psychiatric illness. Moreover, increased HPA activity in adulthood was significantly related to poor childhood adjustment to parental loss. The implications of the results of these studies are discussed.
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PMID:A.E. Bennett award paper. Experimental approaches to human stress research: assessment of neurobiological mechanisms of stress in volunteers and psychiatric patients. 255 97

We assessed the effect of parental loss during childhood on the development of psychopathology in 90 adults. The subjects with a history of adult psychopathology (PATH group), in comparison with subjects with no history of a psychiatric disorder (NO PATH group), had poorer quality of childhood home life and personal adaptation subsequent to parental loss as assessed by the Home Life and Personal Adaptation (HAPA) scale developed by us. Total HAPA scale scores were the single most powerful predictor of adult psychopathology, accounting for correct prediction of adult psychopathology in 80% (72/90) of the subjects. The PATH subjects had significantly increased plasma levels of cortisol and beta-endorphin immunoreactivity. Moreover, cortisol and adrenocorticotropic hormone levels significantly correlated with total HAPA scores. First-degree family history of psychiatric disorders, age at loss, and parental vs maternal loss were not significantly different between PATH and NO PATH subjects. We conclude that the quality of home life subsequent to early parental loss is critically related to the development of adult psychopathology. The hypothesis that early trauma results in enduring neuroendocrine alterations in hypothalamic-pituitary-adrenal axis function is examined.
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PMID:Early parental loss and development of adult psychopathology. 297 65

The evidence for stress activation of endorphinergic systems suggests a physiological role in endogenous analgesic and anti-anxiety regulation which would provide a reserve in emergency situations. The possibility of involvement of these systems in psychiatric illness arises from the psychotogenic and anxiolytic properties of some opiates. The endorphin-excess and -deficiency hypotheses of schizophrenia are reviewed in the light of naloxone's small but statistically significant antipsychotic action, and the activation of endorphinergic systems in the course of neuroleptic therapy. The hypothesis that endorphinergic deficiency may be present in endogenous depression is reviewed. Although alterations in beta-endorphin immunoreactivity measured peripherally and in CNS have not been substantiated, therapeutic trials using a mu-receptor agonist have shown promise of a rapidly-acting antidepressant effect. ECT is accompanied by increases in plasma beta-endorphin immunoreactivity.
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PMID:Endorphins in psychiatry. 609 Oct 98

This study compared basal concentrations of plasma beta-endorphin/beta-lipotropin-like immunoreactivity and dexamethasone suppression of cortisol in seven chronic pain patients, seven psychiatric disorder patients, and seven normal volunteers. Pain patients and psychiatric patients showed significantly higher basal concentrations of beta-endorphin/beta-lipotropin-like immunoreactivity compared to normal volunteers. Pain patients also had significantly higher beta-endorphin/beta-lipotropin-like immunoreactivity than psychiatric patients, even though there was no significant difference in severity of depressive symptomatology as assessed by Beck and Hamilton scores. Resistance to dexamethasone occurred in 57% of pain patients. These results may indicate that biological markers for depression occur in populations of chronic pain patients, or may reflect levels of central nervous system arousal in response to stress, pain, or nonaffective phenomena.
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PMID:Plasma measures of beta-endorphin/beta-lipotropin-like immunoreactivity in chronic pain syndrome and psychiatric subjects. 631 90

Corticotropin-releasing factor (CRF) is a newly sequenced neuropeptide thought to be a principal stimulus to pituitary corticotropin (ACTH) secretion. Evidence obtained from laboratory animals and primates is reviewed which indicates that CRF not only stimulates the pituitary-adrenal axis but also influences several aspects of CNS function which may be of relevance to psychiatric illness. Clinically, experience in administering ovine CRF to more than 150 individuals shows that CRF can be helpful in resolving differential diagnostic dilemmas in patients with various disorders of the hypothalamic-pituitary-adrenal axis and in furthering an understanding of the pathophysiology of conditions such as Cushing's disease and depression.
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PMID:Psychiatric implications of basic and clinical studies with corticotropin-releasing factor. 632 97

Endogenous depression (ED) is regarded as a psychiatric disease with a biological pathogenesis. Consequently patients with ED respond favourably to somatic treatment, whereas for non-endogenously depressed patients drug-treatment would be often inappropriate. Until now, psychopathologists have failed to define precisely the endogenous subtype of depression on clinical features alone. It is well established that a subgroup of depressed patients shows hypersecretion of cortisol and consequently inadequate suppression of cortisol after a test dose of dexamethasone. This dexamethasone suppression test (DST) was introduced as a laboratory marker, specifically identifying endogenously depressed individuals. This survey illustrates the present dispute about the diagnostic confidence and clinical value of the DST in a psychiatric population, and related biochemical aspects. The following conclusions are stated: (a) use of the DST to validate a theory of nosology is premature. (b) Influence of psychoactive drug medication, diet and weight loss have to be established. (c) Preliminary data suggest that abnormal DST results frequently normalize before clinical recovery and abnormal DST results may be observed before a relapse into depression is clinically apparent. From this it was concluded that the DST might be useful as predictor of clinical outcome. (d) From the association of depressive episodes with disinhibited HPA-activity, a causative role of corticotropin and glucocorticoids in the development of psychiatric illness can be hypothesized. Beside some pharmacological data no supportive evidence for this hypothesis is available. (e) Multisteroid analysis after dexamethasone has provided promising results indicating increased sensitivity of the test when based upon cortisol/11-deoxycortisol ratios and disturbed mineralocorticosteroid secretion in endogenously depressed patients.
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PMID:The dexamethasone suppression test in depressed patients: clinical and biochemical aspects. 688 61

To assess the function of the hypothalamus-pituitary-adrenal axis in patients with severe premenstrual syndrome (PMS) 28 patients and 14 asymptomatic controls were studied during the mid- to late-luteal phase of the menstrual cycle. The response of plasma cortisol to both high-dose naloxone and corticotropin-releasing hormone (CRH) was assessed. Naloxone stimulated a significant cortisol release in controls whereas it was otherwise almost absent in patients. CRH stimulated a greater release of cortisol in patients than in controls. Fifteen patients met criteria for either current anxiety and/or mood disorders. The cortisol secretion after both naloxone and CRH stimulations was similar for PMS patients with or without psychiatric disorders. These data indicate that endogenous opioids modulate the activity of the hypothalamus-pituitary-adrenal axis. Irrespective of the concomitant presence of menstrual migraine or psychiatric disorder, such control is altered in patients with severe PMS because of the possible hyposensitivity of opiate receptors. The hyperresponsiveness to CRH may be the consequence of the reduced inhibition that endogenous opioids tonically exert on HPA axis.
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PMID:Changes of opioid modulation of the hypothalamo-pituitary-adrenal axis in patients with severe premenstrual syndrome. 780 41

In a previous study, increased weight of the adrenal glands was found in a small group of persons who committed violent suicides. This finding was confirmed in our study, which comprised a group of 42 suicide cases and 37 control cases. Further analysis with special consideration toward a "relative adrenal weight" (weight/body surface) revealed that a relative combined adrenal weight >6 g/m2 may be a morphologic sign of a depressive disorder prior to death if no other disease with a known effect on the adrenals is present. These results are consistent with clinical computed tomographic findings of enlarged adrenals in depressed patients. In all suicide cases the police records were reviewed and a postmortem psychiatric diagnosis conducted to investigate whether a correlation between adrenal weight and the "severity" of depression or type of psychiatric disorder exists. In thirteen cases, psychiatric treatment prior to death was known, and a postmortem severity score of depressive disease was formed. No influence of this score or the postmortem diagnosis on the adrenal weight, however, could be detected. Also, the increase in weight of adrenal glands could not be explained by a suspected or proven preceding drug therapy or use. The effect on the pituitary-adrenal-axis by depressive disorders and changes in serotonin metabolism have been investigated repeatedly; mainly reported are increased levels of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) in the depressive interval, which may lead to a growth of the adrenal glands.
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PMID:Weight of adrenal glands may be increased in persons who commit suicide. 953 97


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