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)

Cerebrospinal fluid hormones, monoaminergic metabolites, and dynorphin A (1-8 sequence) were examined in 43 children with severe, primary obsessive-compulsive disorder. Cerebrospinal fluid levels of 5-hydroxyindoleacetic acid were positively correlated with one of eight obsessive-compulsive disorder severity ratings and three of seven measures of improvement following 5 weeks of treatment with clomipramine hydrochloride. Arginine vasopressin concentration was significantly and negatively correlated with several ratings of obsessive-compulsive disorder symptom severity, while oxytocin concentration was positively correlated with depressive symptoms. The ratio of arginine vasopressin to oxytocin was also negatively correlated with obsessive-compulsive disorder and depressive symptoms. Comorbid affective disorder was associated with decreased arginine vasopressin concentrations, while concomitant anxiety disorder was associated with increased oxytocin. Dynorphin A (1-8 sequence), homovanillic acid, corticotropin, 3-methoxy-4-hydroxyphenylglycol, and corticotropin releasing hormone were not significantly related to obsessive-compulsive disorder symptoms. These results seem to indicate that arginine vasopressin may be related to obsessive-compulsive disorder symptom severity, while 5-hydroxyindoleacetic acid might be associated with drug response.
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PMID:Cerebrospinal fluid neurochemistry in children and adolescents with obsessive-compulsive disorder. 137 Jan 97

In humans who chronically abuse amphetamine (AMPH), sudden abstinence often precipitates an organic mood disorder that mimics many symptoms of major depression. We report that AMPH exposure and withdrawal in rats modifies hypothalamic-pituitary-adrenal axis endocrine responses, peripheral immune functions, and regional brain catecholamine levels. Compared to vehicle-treated animals, rats treated with AMPH for 10 days exhibit significantly decreased physostigmine-induced release of adrenocorticotropin hormone (ACTH). During AMPH withdrawal, these animals show a loss of the normal correlation between levels of plasma ACTH and corticosterone. Chronic AMPH treatment in rats causes a significant increase in natural killer cell activity. Brain dopamine levels in these animals are decreased in the caudate nucleus but are increased in the nucleus accumbens. AMPH withdrawal in rats may be a useful model for studying the physiologic and neural substrates of human AMPH withdrawal states.
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PMID:Endocrine, immune, and neurochemical changes in rats during withdrawal from chronic amphetamine intoxication. 165 16

The neurohumoral changes induced by electroconvulsive therapy (ECT) in pregnancy have not been described previously. In the nonpregnant adult, ECT causes an acute rise in prolactin, adrenocorticotropic hormone (ACTH), cortisol, norepinephrine, epinephrine and beta-endorphin. Because pregnancy alters the production and release of these hormones, consideration should be given to how ECT may further alter the neuroendocrine response, with possible implications for the success of treatment and the fetal response. A 30-year-old woman with a major affective disorder underwent a course of ECT beginning at 23 weeks' gestation. Serial hormonal assays of peripheral venous samples from -30 to +240 minutes were obtained during her first treatment. The prolactin, ACTH, norepinephrine, epinephrine, beta-endorphin, dopamine and oxytocin levels rose acutely and returned to baseline during observation. The maternal vital signs were stable. No increase in uterine activity or fetal heart rate abnormalities were observed during any treatment. A healthy infant weighing 2,900 g was delivered at term, with Apgar scores of 9 and 9 and no problems. We conclude that there are acute neurohumoral changes in specific hormones with ECT in pregnancy, but none of these changes appeared to adversely affect the fetus in our case.
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PMID:Acute neurohumoral response to electroconvulsive therapy during pregnancy. A case report. 257 26

Twenty-three patients with pituitary adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome were studied before and after treatment. The relationship between the amelioration of the depressive syndrome and changes in cortisol and ACTH levels was investigated. There was a significant difference in mean change in 24-hour urinary free cortisol (UFC) excretion for changes in the depressed mood score from first to last visit. There were also significant correlations between decreases in UFC and decreases in both the depressed mood score and the modified Hamilton depression score. These relationships were not found for ACTH. Furthermore, with cortisol decreased to normal levels, continued high ACTH levels did not prevent improvement in depressed mood. The possibility that cortisol may also play a role in the pathogenesis and/or maintenance of the mood disorder in psychiatric patients is discussed.
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PMID:Cushing's syndrome after treatment: changes in cortisol and ACTH levels, and amelioration of the depressive syndrome. 302 5

Immunoreactive plasma beta-endorphin level was assayed in 33 patients with major affective disorder and in 16 psychiatrically normal controls before and after dexamethasone (1 mg) administration at 23.00 h. There were 18 cortisol suppressors and 15 non-suppressors among the patient group. All controls suppressed cortisol. Plasma beta-endorphin before dexamethasone was significantly different between suppressors, non-suppressors and controls (P less than 0.05, ANOVA). Concentrations of beta-endorphin were 4.7 +/- 0.7, 3.1 +/- 0.3 and 2.8 +/- 0.3 pmol/l for non-suppressors, suppressors and controls respectively. Following dexamethasone, beta-endorphin concentrations were again significantly different between groups (P less than 0.005, ANOVA). Concentrations were 4.6 +/- 0.7, 2.3 +/- 0.2 and 1.6 +/- 0.2 pmol/l for non-suppressors, suppressors and controls respectively. The implications of these findings are discussed.
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PMID:Plasma immunoreactive beta-endorphin in dexamethasone suppressors and non-suppressors of cortisol. 303 84

To study the pathophysiology of hypercortisolism in anorexia nervosa, we measured the cerebrospinal fluid (CSF) levels of corticotropin-releasing hormone (CRH) in patients when they were underweight and at intervals after weight restoration. CSF CRH levels were significantly elevated in hypercortisolemic underweight patients. Both CSF CRH levels and pituitary-adrenal function normalized after weight recovery. A significant positive correlation was found between CSF CRH levels and depression ratings in weight-corrected patients. We conclude that the hypercortisolism of anorexia nervosa reflects a defect at or above the hypothalamus which results in the hypersecretion of endogenous CRH. The positive correlation between CSF CRH and depression in the weight-restored patients is compatible with previous data indicating increased CRH secretion in the depressed phase of primary affective disorder and supports the notion of a relationship between CRH and depressive symptomatology. Moreover, these data are compatible with observations that depression is part of the anorexia nervosa syndrome.
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PMID:Elevated cerebrospinal fluid levels of immunoreactive corticotropin-releasing hormone in anorexia nervosa: relation to state of nutrition, adrenal function, and intensity of depression. 349 30

The authors present a case report that provides support for a relationship between estrogen and the menstrual cycle on the 1 hand and affective disorders on the other. The patient in this case, a 35-year old woman, suffered from a rapid cycling affective disorder that was severely affected by her menstrual cycle and responded positively to oral contraceptives (OCs). The patient had a 24-year history of numerous manic and depressive episodes, the 1st of which coincided with menarche. She had noted that, 4 days before menses, she would experience symptoms of premenstrual tension syndrome (PMS) and often the onset of an affective episode. Treatment with a series of psychotropic agents had not been effective in controlling the number of episodes. However, the patient reported that there had been an 8-9-month period in the past when she had taken OCs and had fewer symptoms. Thus, the patient was placed on Ortho-Novum as well as imipramine. At the 9-month follow-up, she reported there had been no further episodes of depression or mania. The exact mechanism behind estrogen's psychotropic effect is unclear, although it increases the central availability of norepinephrine and induces changes in dopaminergic, noradrenergic, and serotonergic receptors. Beta-endorphin levels covary with estrogen levels, and estrogen seems to affect every major neurotransmitter system. The fact that estrogen has not consistently been shown to be effective in this regard may only signify the existence of a distinct subclass of affective disorders closely linked to the menstrual cycle. This subclass may have some type of dysfunction within the hypothalamic-pituitary-gonadal axis that contributes to mood swings.
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PMID:Antidepressant effects of estrogen. 405 18

We investigated the relationship between hypothalamic-pituitary-adrenal (HPA) activity, as measured by 24-hour mean urinary free cortisol (MUFC), and cerebrospinal fluid (CSF) opioid activity in patients with major affective disorder and normal volunteers. Among depressed patients, but not normal volunteers, mean 24-hour urinary cortisol values were significantly correlated with CSF opioid activity measured by radioreceptor assay, but were not significantly correlated with beta-endorphin immunoreactivity measured by radioimmunoassay. MUFC, as expected, was significantly higher in depressed patients than in normal volunteers. Mean values of CSF opioid activity and beta-endorphin immunoreactivity did not differ significantly in the two groups. The positive opioid-MUFC correlation found in the depressed group appeared to depend on patients who were cortisol hypersecretors. These data, using relatively crude measures of cortisol and opioid activity, are suggestive of a relationship between these two systems, particularly under "activated" conditions such as those observed in depression.
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PMID:Relationship between urinary free cortisol and CSF opioid binding activity in depressed patients and normal volunteers. 626 42

Morning plasma concentrations of beta-endorphin immunoreactivity were significantly higher in a group of depressed patients meeting the Research Diagnostic Criteria for Major Depressive disorder or Schizo-affective disorder, depressed, than in age- and sex-matched groups of normal controls and psychiatric patients without affective disorders. Furthermore, physostigmine-stimulated release of beta-endorphin immunoreactivity was also significantly greater in the depressed patients. These results provide the first evidence for elevated plasma concentrations of beta-endorphin in depression and also represent further evidence for cholinergic supersensitivity in depression. These results suggest that elevated plasma concentrations of beta-endorphin and cholinergically stimulated hypothalamic-pituitary beta-endorphin release, might potentially represent biological state or trait markers for depression.
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PMID:beta-Endorphin hypersecretion in depression: possible cholinergic mechanisms. 629 94

The purpose of this article is to review the literature on the effects of the menstrual cycle on dependent variables in mood disorder research to inform investigators which physiological measures are likely to be significantly affected by menstrual cycle fluctuations and precisely how they might be affected. The following variables are discussed: prolactin; growth hormone; the hypothalamic-pituitary-thyroid axis (including thyrotropin, triiodothyronine, and thyroxine); the hypothalamic-pituitary-adrenal axis (cortisol, corticotropin, and beta-endorphin); melatonin; sleep; body temperature; and neurotransmitter activity (serotonergic and adrenergic systems). Body temperature and plasma and urinary norepinephrine vary predictably over the menstrual cycle. Prolactin and beta-endorphin may have peaks in the periovulatory phase, whereas serotonin levels in platelet-poor plasma may reach a nadir at that time. Triiodothyronine, thyroxine, cortisol, and melatonin do not appear to vary systematically over the course of the menstrual cycle, whereas the data for growth hormone, thyrotropin, corticotropin, and sleep are inconclusive.
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PMID:Effects of the menstrual cycle on dependent variables in mood disorder research. 759 37


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