Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was aimed at investigating the relationship between "chronic constitutional tetany" (spasmophilia) and headache. Several adult patients presenting with neuromuscular hyperexcitability, anxiety, dysautonomia, and oculofrontal headache were subjected to a series of ion and hormone blood tests, and the results were compared with those in control subjects. Calcium and parathyroid hormone levels were significantly decreased, and phosphorus and beta-endorphin-like immunoreactivity were significantly increased. A subgroup of the patients had all four abnormalities. In most cases the family history was positive for headache. Sleep disturbances and personal histories of periodic syndrome in infancy were recorded. It is concluded that a correlation may exist between the symptoms assessed and an impairment of some ion and hormone levels. There are several traits in common with "common migraine", and our patients may form a subgroup of that group. A possible linkage between headache/tetany and the periodic and hyperventilation syndromes is discussed. The increased beta-endorphin-like immunoreactivity is putatively a reactive phenomenon.
...
PMID:Calcium deficiency and supraorbital headache: a clinical study of adult subjects. 294 51

It is well established that corticotropin-releasing factor (CRF), a peptide comprised of 41 amino acids, is the major physiological regulator of the pituitary-adrenal axis by virtue of its role as the hypothalamic hypophysiotropic hormone that modulates the secretion of adrenocorticotropin (ACTH) from the anterior pituitary gland. In addition to its neuroendocrine role, CRF appears to function as a neurotransmitter or neuromodulator in extrahypothalamic brain areas. The peptide and its receptors are distributed throughout the central nervous system (CNS), and CRF is released by depolarizing concentrations of potassium in a calcium-dependent manner. After direct CNS administration, CRF produces a number of behavioral and physiological effects that are reminiscent of both an organism's response to stress and to the symptoms of patients with major depression. These include: diminished food consumption, decreased sexual behavior, disturbed sleep, alterations in locomotor activity and sympathetic nervous system activation. Alterations in regional brain CRF concentration in rats were observed after acute and chronic stress, i.e. decreased hypothalamic and increased locus coeruleus CRF concentrations. To test the hypothesis that CRF is hypersecreted in patients with major depression, the concentration of CRF in cerebrospinal fluid (CSF) in drug-free depressed patients and age- and sex-matched controles was measured in two studies. The depressed patients exhibited a clear group-related increase in CSF CRF concentrations. To further test this hypothesis that CRF is chronically hypersecreted in depressed patients, the number and affinity of CRF receptors in frontal cortex was measured in a group of suicides and age-matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The role of corticotropin-releasing factor in the pathogenesis of major depression. 329 91

The present study was designed to investigate the clinical efficacy of trimipramine with adjunct sleep deprivation (SD) or bright light (BL) and to evaluate psychometric and neurobiological variables that might be of predictive value for treatment response. We used (1) the combined dexamethasone-corticotropin releasing hormone test (DEX-CRH test) to characterize alterations of the hypothalamic-pituitary-adrenal (HPA) system; (2) polysomnography to evaluate sleep disturbances; and (3) a standardized test battery to assess cognitive psychomotor functions after study initiation and after 5 weeks of treatment. The overall response rate (> or = 50% decrease in score on Hamilton Rating Scale for Depression [HRS]) was 55% (N = 42). The response rate in the group with trimipramine monotherapy (N = 14) was 79%, whereas in the groups with adjunct SD (N = 14) and BL (N = 14), respectively, it was only 43%. All three groups showed significant improvement at the end of the third week of treatment. Neither of the adjunct treatments hastened the onset of antidepressant action as measured by HRS. A significantly higher proportion of nonresponders than responders (p < .05) had HPA dysregulation, disturbed rapid eye movement (REM) sleep (REM latency, REM% first third of night) and decreased non-REM sleep (% stage 2). The non-responders showed significantly more corticotropin (ACTH) secretion after CRH stimulation in the DEX-CRH test than the responders and a less rapid normalization of the neuroendocrine dysregulation (cortisol secretion) (p < .01). In addition, REM latency was significantly shorter in the BL group than in the monotherapy group and estimated duration of illness significantly longer in the SD group than in the monotherapy group. REM latency, percentage of REM sleep during the first third of the total sleep period, percentage of non-REM sleep stage 2 and ACTH release after a DEX-CRH challenge predicted response across all three treatment groups. The neurobiological symptoms were unevenly distributed, among the three groups, thus creating heterogeneity in these measures. This heterogeneity may have contributed to the different treatment response rates as defined by psychopathology (HRS). In contrast, the neuropsychological tests and some of the sleep-EEG investigations revealed different response patterns for different groups: The onset of improvement in simple cognitive functions and in sleep continuity was earlier in the adjunct treatment groups. This study underlines the need for a multidimensional approach including use of neurobiological and neuropsychological measures to identify the therapeutic profiles of different treatment strategies and predictors of outcome.
...
PMID:Sleep deprivation and bright light as potential augmenters of antidepressant drug treatment--neurobiological and psychometric assessment of course. 787 17

Human sleep is characterized by the cyclic occurrence of nonREM and REM periods and by distinct patterns of nocturnal hormone secretion. A host of factors may result in disturbed sleep, including normal aging and depression. In both states, similar changes in sleep-endocrine activity occur, including decreases in slow wave sleep and in growth hormone secretion. Preclinical investigations and studies by our laboratory in young and elderly normal controls and in patients with depression demonstrate that neuropeptides play a key role in sleep regulation. As an example, growth hormone-releasing hormone (GHRH) is a common stimulus of slow wave sleep and growth hormone release, whereas corticotropin-releasing hormone (CRH) exerts opposite effects. We suggest that an imbalance of both peptides in favor of CRH contributes to changes in sleep-endocrine activity during depression and aging.
...
PMID:[Physiology and pathophysiology of sleep]. 853 82

Sleep disturbances are an integral feature of depressive disorders. Like the disorders themselves, the sleep disturbances associated with depression are heterogeneous, ranging from hypersomnia to marked difficulties maintaining sleep. These difficulties are to some extent age dependent and reflect abnormalities of central nervous system arousal. Moreover, the sleep disturbances associated with depression have both reversible, or state-dependent, and more persistent trait-like characteristics. Polysomnographic recordings can be used to document sleep maintenance difficulties, and they often also reveal reduced slow wave sleep, an early onset of the first episode of rapid eye movement (REM) sleep, and increased phasic REM sleep. A deficit of serotonergic neurotransmission, a relative increase in pontine cholinergic activity, and, perhaps, an excess of noradrenergic and corticotropin-releasing hormone activity have been implicated in the pathogenesis of the sleep disturbances of more severe depressive disorders. Antidepressant medications have class- and compound-specific effects on polysomnographic profiles. Unlike other antidepressants, bupropion may increase or intensify REM sleep. While no single effect of antidepressants on sleep neurophysiology is necessary or sufficient for treatment efficacy, differences in drug effects may provide important clues to selection of specific medications for particular patients.
...
PMID:Depression, sleep, and antidepressants. 955 22

Various peptides including corticotropin-releasing hormone (CRH) exert selective effects on sleep structure and noctural secretions of cortisol and growth hormone (GH). In animal studies analeptic effects and sleep disturbances after thyrotropin-releasing hormone (TRH) administration have been observed; studies of endocrine function in depressed patients suggest a pathological activity of CRH and TRH as compared with that in healthy volunteers. As the role of TRH in the regulation of the sleep endocrine pattern in humans has not yet been clarified, we performed a study to examine the effects of pulsatile administration of TRH on the sleep EEG pattern and the nocturnal secretions of cortisol and GH in 7 healthy male subjects. The sleep EEG was recorded from 23.00 to 07.00 h, and blood samples were collected every 20 min from 20.00 to 07.00 h for the analysis of GH and cortisol concentrations during intravenous administration of placebo or 4 x 50 microgram TRH at 22.00, 23.00, 24. 00, and 01.00 h. In contrast to the well-known effects of CRH on the sleep endocrine pattern, TRH exerts only a weak effect on the sleep EEG which is reflected in a slight decrease in sleep efficiency associated with a trend to wakefulness during the night. Furthermore, after TRH administration, the cortisol rise appeared earlier, and a nonsignificant tendency to an increased secretion of cortisol during the first half of the night was found. The GH secretion did not differ significantly after application of TRH or placebo. The activating, albeit weak, effect of TRH on the sleep EEG and nocturnal cortisol secretion in healthy volunteers confirms and adds to the results previously observed in animals. On the basis of these findings, we surmise that TRH may contribute to the disturbed sleep continuity seen in depressed patients, probably acting as a cofactor of CRH in a synergistic manner.
...
PMID:Effects of thyrotropin-releasing hormone on the sleep EEG and nocturnal hormone secretion in male volunteers. 970 19

Anxiolytic and sedative effects of neuropeptide Y (NPY) are thought to involve inhibition of corticotropin-releasing hormone (CRH). Enhanced secretion of CRH plays a critical role in the pathophysiology of major depression, characterized by sleep disturbances, anxiety and loss of appetite. We examined for the first time in young men effects of intravenous injections of NPY (4x50 or 100 microg, n = 9 and 11, respectively, at 22.00, 23.00, 24. 00 and 01.00 compared to saline) on the sleep electroencephalogram (EEG; recorded from 23.00 to 07.00) and nocturnal secretion of adrenocorticotrophic hormone (ACTH), cortisol, growth hormone (GH), prolactin and leptin. Repeated measures MANOVA showed that ACTH secretion during the first half of the night was reduced by the lower dose of NPY only (F = 8.7, p<0.05), while cortisol secretion during the second half of the night was reduced regardless of the dose (F = 7.9, p<0.05). Regardless of the dose, NPY enhanced sleep period time and stage 2 sleep (F = 12.8 and 5.4, each p<0.05), and also reduced sleep latency and time awake (F = 4.9 and 4.4, each p<0.05) and modulated REM sleep. In summary, NPY promotes sleep and inhibits the hypothalamo-pituitary-adrenocortical (HPA) axis in humans, pointing to a possible role of NPY agonists for the development of novel treatment strategies for affective disorders.
...
PMID:Neuropeptide Y promotes sleep and inhibits ACTH and cortisol release in young men. 1081 63

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
...
PMID:Cytokine dysregulation, inflammation and well-being. 1616 5

Sleep electroencephalographic (EEG) abnormalities and increased hypothalamo-pituitary-adrenal (HPA) axis activity are the most prominent neurobiological findings in depression and were suggested as potential biomarker for depression. In particular, increased rapid eye movement sleep (REM) density, deficit in slow wave sleep and excessive stress hormone response are associated with an unfavorable long-term outcome of depression. Recent studies indicate that the sleep and endocrine parameters are related to each other. This study investigated the association of sleep structure including a quantitative EEG analysis with the results of the combined dexamethasone (Dex)/corticotropin-releasing hormone (CRH)-test in 14 patients with a severe major depression, 21 healthy probands with a positive family history of depression (HRPs) and 12 healthy control subjects without personal and family history for psychiatric disorders. As expected patients with depression showed an overactivity of the HPA axis, disturbed sleep continuity and prolonged latency until slow wave sleep in the first sleep cycle. Differences in microarchitecture of sleep were less prominent and restricted to a higher NonREM sigma power in the HRP group. Dexamethasone suppressed cortisol levels were positively associated with higher NonREM sigma power after merging the three groups. We also observed an inverse association between the ACTH response to the Dex/CRH-test and rapid eye movement sleep (REM) density in HRPs, with suggestive evidence also in patients, but not in controls. This contra-intuitive finding might be a result of the subject selection (unaffected HRPs, severely depressed patients) and the complementarity of the two markers. HRPs and patients with high disease vulnerability, indicated by an elevated REM density, seem to have a lower threshold until an actual disease process affecting the HPA axis translates into depression, and vice versa. To summarize, our findings provide further evidence that the HPA axis is involved in the sleep regulation in depression. These associations, however, are not unidimensional, but dependent on the kind of sleep parameters as well as on the selection of the subjects.
...
PMID:Dex/CRH-test response and sleep in depressed patients and healthy controls with and without vulnerability for affective disorders. 1828 Oct 62

It is widely accepted that orexin (hypocretin) bears wake-promoting effects. While under normal conditions the circadian rhythm of orexin release has a clear circadian distribution, the amplitude of orexin fluctuation is dampened in depression. Interestingly, clinical symptoms of depression include several sleep disturbances. In this disease, corticotropin-releasing hormone (CRH) seems to be another factor influencing sleep. As neurophysiological interactions and anatomical connections between the orexinergic and the CRH system point to mutual influences of these two neuropeptides, we examined whether a dysfunctional CRH-receptor system in two different CRH receptor knock out models alters general wake-promoting effects of orexin applied exogenously. Orexin was injected intracerebroventricularlly into CNS-restricted CRH-receptor type 1 knockout mice (CRH-R1 KO) and CRH-receptor type 2 knockout mice (CRH-R2 KO) and baseline sleep was recorded from the freely behaving mice. A third experiment included antisauvagine-30 injections (CRH-R2 antagonist) into CRH-R1 KO animals. Orexin had similar wake-promoting effects in CRH-R1KO mice, in CRH-R2 KO animals and in CRH-R1KO mice treated with antisauvagine-30. Consistent results were obtained from all corresponding control littermate experiments. According to our results we conclude that the wake-promoting effects of orexin are not influenced by a possible contribution of CRH.
...
PMID:Wake-promoting effects of orexin: Its independent actions against the background of an impaired corticotropine-releasing hormone receptor system. 2142 Apr 42


1 2 Next >>

---