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)

Advances in neuropeptide neurobiology in the last decade are illustrated by studies of corticotropin-releasing factor (CRF), the 41 amino acid-containing peptide that controls the anterior pituitary secretion of adrenocorticotropin and other pro-opiomelanocortin products. Corticotropin-releasing factor is synthesized in both hypothalamic and extrahypothalamic perikarya in a large prohormone form, (186 amino acids), then it is processed and transported to nerve terminals where it is released in its active form by a calcium-dependent mechanism. Corticotropin-releasing factor biosynthesis can now be measured by in situ hybridization because of the elucidation of the CRF gene sequence. Once released, CRF acts on high-affinity CRF receptors, and signal transduction is mediated by activation of adenylate cyclase in certain brain areas, and perhaps by phosphoinositide hydrolysis. In other brain areas CRF is inactivated by peptidases that degrade the hormone, though these are not well characterized. A CRF binding protein has been identified in plasma, and perhaps in brain. Considerable evidence exists from cerebrospinal fluid studies, postmortem tissue receptor measurements, and CRF stimulation test studies to support the hypothesis that CRF is hypersecreted in depression, resulting in both pituitary-adrenal axis hyperactivity and certain signs and symptoms of depression, e.g., decreased libido, insomnia, and decreased appetite. There is also evidence for an involvement of CRF in the pathophysiology of anxiety disorders and in the mechanism of action of benzodiazepines. The development of selective CRF-receptor antagonists will permit direct testing of the hypothesis that CRF hypersecretion is responsible for certain of the cardinal features of affective and anxiety disorders.
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PMID:New vistas in neuropeptide research in neuropsychiatry: focus on corticotropin-releasing factor. 161 Apr 87

Apomorphine (Apo), a D1/D2 Dopamine (DA) agonist, at high doses (500 micrograms/kg) induces a short-lasting insomnia, antagonized by a secondary injection of corticotropin-like intermediate lobe peptide (CLIP, 10 ng); these effects are also observed with hypophysectomized (hypoX) rats. The administration of the serotonin (5-HT) agonist 8-hydroxy-2-di-n-propylamino-tetralin (8-OHDPAT, 0.3 mg/kg) induces also an insomnia which, unlike Apo, is followed by a significant PS rebound. CLIP, again, antagonizes the 8-OHDPAT-induced insomnia. Finally, Bromocriptine (5 mg/kg), an agonist for both DA and 5-HT, induces first an insomnia (antagonized by CLIP), followed by a PS rebound; these effects persist in hypoX rats.
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PMID:Proopiomelanocortin (POMC)-derived peptides and sleep in the rat. Part 2--Aminergic regulatory processes. 196 3

A yin-yang hypothesis is presented linking noradrenergic activity, thromboxane, melatonin, left hemisphere functioning, and cyclic AMP on the one hand, and dopamine, beta-endorphin, calcium, right hemisphere functioning, and cyclic GMP on the other. It is further suggested that there is a yoking of NA, TXA2, serotonin and melatonin in the left hemisphere, and a similar yoking of DA, BE, calcium and cGMP in the right. Evidence is presented to support the hypothesis that each element (NA, TXA2, etc.) on one side can modulate or balance a corresponding element (DA, BE, etc.) on the other. It is suggested that thromboxane is the key element in noradrenergic overactivity and that not taking this into consideration has confounded much prior research. This theory takes into account information processing models as well as pharmacological data and neurochemical theory on coupling of adenylate cyclase to its hormone receptors. Inhibiting noradrenergic overactivity can be obtained by inhibiting thromboxane and concomitantly activating opiate receptors. This protocol may have clinical utility in treating a wide range of disorders such as: anxiety, depression, schizophrenia, sleeplessness, withdrawal states, enuresis, Gilles de la Tourette syndrome, Parkinsonism, Alzheimers, dementia, anorexia, infant ruminations, essential tremor, spasticity of spinal cord injury, diarrhoea, ulcerative colitis, extrapyramidal symptoms, akathisia, neuroleptic malignant syndrome, attention deficit disorder, hyperhidrosis, and possibly AIDS.
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PMID:Inhibiting noradrenergic overactivity by inhibition of thromboxane and concomitant activation of opiate receptors via dietary means. 254 22

While prolonged loss of sleep is unpleasant and demanding, it remains unclear if it blunts or enhances the physiological stress imposed by subsequent exercise. To investigate this, we deprived eight subjects of sleep prior to exercise to see if this altered the stress hormonal response to that exercise. In a first series of experiments, two fragmented nights of sleep preceded 30 min of heavy treadmill walking exercise. While sleep loss disturbed mood before and during exercise (p less than 0.05), it left stress hormonal levels (cortisol and beta-endorphin) in blood identical to control. In a second series, subjects performed light treadmill walking exercise for 3 h after 36 sleepless hours. As before, sleep deprivation disturbed mood before and throughout exercise (p less than 0.05), but failed to change blood levels of stress hormones. In both series, sleeplessness left heart rate, oxygen uptake, minute ventilation, and body core temperature unchanged in exercise. We conclude that sleep loss provokes psychological changes during subsequent exercise without measurably altering the stress hormonal response to that exercise.
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PMID:Stress hormonal response to exercise after sleep loss. 293 42

Thirty-five consecutive patients with Cushing's syndrome were studied prospectively before treatment. A consistent constellation of neuropsychiatric disturbances was found, including impairments in affect (depressed mood and crying), cognitive functions (decreased libido and insomnia). Thirty-four percent of patients were rated as having a mild, 26% a moderate, 29% a severe, and 11% a very severe psychiatric disability. A statistically significant relationship was found between the overall neuropsychiatric disability rating and cortisol and adrenocorticotropic hormone (ACTH) levels. Patients with adrenal adenomas with high cortisol but low ACTH levels did not have as severe a neuropsychiatric disability.
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PMID:Neuropsychiatric manifestations of patients with Cushing's syndrome. Relationship to cortisol and adrenocorticotropic hormone levels. 625 94

The effects of beta-endorphin and of morphine SO4 (0.5 microgram and 2.0 microgram, respectively, injected intraventricularly) upon the sleep-wakefulness behavior of cats were examined. Both agents produced insomnia. Deep slow wave sleep was sharply inhibited, and rapid eye movement (REM) sleep was entirely suppressed. Light slow wave sleep, occurring in brief, isolated episodes, became the most abundant stage of sleep. The nuchal electromyogram was markedly increased after both agents. Naloxone (100 microgram/kg), injected subcutaneously 30 min before beta-endorphin or morphine SO4, entirely reversed these agents' effects on the two stages of slow wave sleep, and antagonized the exaggerated electromyogram. But naloxone did not counteract the REM-suppressant effect of either beta-endorphin or morphine SO4. Total sleep time reverted towards control values after naloxone pretreatment, but not entirely; the difference may be due to the persistent deficit of REM sleep. The data may indicate an involvement of an inner opioid in the regulation of sleep and wakefulness in the cat, and may point to a role for more than one endorphin receptor in the effects of opioids on the states of vigilance in cats.
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PMID:Effects of beta-endorphin and morphine on the sleep-wakefulness behavior of cats. 627 85

Thirty-two patients with various severe or selected dermatoses were chosen for treatment with cortisone acetate by mouth. The criteria for selection included refractoriness to previous therapy and absence of ascertainable contraindications. The initial dose of cortisone acetate varied between 100 and 200 mg. per day. The dose was reduced as quickly as each patient's response permitted, with the object of reaching the lowest effective dose as quickly as possible. Response of most patients to the hormone was dramatic, with abatement of symptoms within 24 hours and substantial improvement of clinical signs within 24 to 48 hours. Details of the results are tabulated. Adverse effects, possibly attributable to the hormone, were noted in five patients. In two instances, moon facies developed, one with hypertrichosis and a 20-lb. (9.1-kg.) gain in weight. However, both of these patients had received corticotropin (ACTH) prior to the cortisone. A third patient showed hyperpigmentation of the areas of skin usually exposed and not covered by clothing. Two additional patients each complained of hyperexcitability and insomnia. All these undesirable effects diminished or disappeared after the dose was reduced or administration of cortisone was discontinued. The effectiveness of this new therapeutic approach in a wide variety of skin diseases is clearly demonstrated by the excellent response noted in this series of selected cases. No other modality known to us has comparable beneficial effects. It is to be stressed, however, that the benefits generally stop soon after cortisone therapy is discontinued, unless the disease or the attack is one with spontaneous remissions. Disagreeable and sometimes dangerous effects still preclude the use of this treatment except in serious diseases and situations, and unless the patient can be kept under sufficiently close and expert surveillance.
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PMID:Centennial Paper. November 1951 (Arch Dermatol Syphilol: Cortisone acetate administered orally in dermatologic therapy by Marion B. Sulzberger, Victor H. Witten and Stanley N. Yaffe. 635 55

Two peptides known for their hypnogenic properties, CLIP (corticotropin-like intermediate lobe peptide or ACTH 18-39) or VIP (vasoactive intestinal polypeptide), were injected locally into the nucleus raphe dorsalis (nRD) of rats pretreated with p-chlorophenylalanine (PCPA). During the dark period, the PCPA insomnia was primarily associated with a reduction in paradoxical sleep (PS), whereas both slow wave sleep (SWS) and PS were decreased during the light period. Immunohistochemistry of serotonin in PCPA-pretreated animals indicated a clear disappearance of 5-HT fibers in the basal hypothalamus and the nRD as compared to control animals. Local injections of CLIP or VIP in the nRD restored PS and SWS. The positive injection sites corresponded to the anatomical distribution of either CLIP or VIP fibers, i.e., the entire nRD for VIP and the antero-dorsal part of this nucleus for CLIP. The sleep effects obtained in PCPA-pretreated rats involve a non-5-HT sleep permissive component within the nRD upon which these injected peptides act.
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PMID:Sleep permissive components within the dorsal raphe nucleus in the rat. 758 81

Fatal familial insomnia is a prion disease in which a selective thalamic degeneration leads to total sleep deprivation, hypertension, dysautonomia, adrenal overactivity, and impaired motor functions. With patients under continuous recumbency and polysomnographic control, we assessed the changes in the 24-hour patterns of blood pressure, heart rate, plasma catecholamines, corticotropin, and serum cortisol in three patients at different stages of the disease. Six healthy volunteers were used as control subjects. A dominant 24-hour component was detected at rhythm analysis of all variables, both in patients and control subjects. In the patients, the amplitudes gradually decreased as the disease progressed, leading to the obliteration of any significant dirunal variation only in the preterminal stage. A shift in phase corresponded to the loss of the nocturnal fall in blood pressure in an early stage of the disease, when nocturnal bradycardia was still preserved. Plasma cortisol was high and became increasingly elevated, whereas corticotropin remained within normal levels; abnormal nocturnal peaks appeared in their circadian patterns. The disrupted patterns of cortisol and blood pressure preceded the development of hypertension and severe dysautonomia, which in turn were paralleled by increasing catecholamine and heart rate levels. Our data demonstrate that in patients with fatal familial insomnia the changes detectable in the rhythmic component of diurnal blood pressure variability result in a pattern of secondary hypertension. Disturbances in thalamic, pituitary-adrenal, and autonomic functions seem to be involved in mediating these changes.
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PMID:Diurnal blood pressure variation and hormonal correlates in fatal familial insomnia. 817 63

The model of sleep deprivation in rats by the platform method has been extensively studied in our laboratory as a possible animal model of mania. At the end of the period of sleep deprivation, the rat does not fall asleep as soon as it is returned to its home cage, but shows a period of wakefulness of about 30 min, during which the animal presents a cohort of symptoms that appear to mimic those present in idiopathic mania. In particular, during this period the animal displays insomnia, a high degree of hyperactivity, irritability, aggressiveness, hypersexuality and stereotypy. Haloperidol (0.2 mg/kg) was effective in reducing latency to sleep, while L-sulpiride was much weaker (< 50 mg/kg). The dopamine D1 receptor antagonist SCH 23390 exhibited an extremely high potency and efficacy in reducing sleep latency, a significant effect being observed with 3 micrograms/kg. The administration of the specific D1 receptor agonist SKF 38393 markedly prolonged the period of insomnia with the correlated behavioral syndrome. When lithium was added to the diet and consumed during the sleep deprivation period in adequate amounts to produce serum lithium levels of 0.7-1.0 mEq/l, sleep latency and locomotor activity were significantly reduced. The administration of naloxone (1-10 mg/kg) reduced the latency to sleep in a dose-related manner. By contrast, morphine (1 and 5 mg/kg, i.p.), beta-endorphin and [D-Ala2,D-Leu5]enkephalin (i.c.v., 2 and 1 micrograms, respectively) markedly prolonged the insomnia. The model not only represents a confirmation in the rat that sleep loss often precedes and may trigger a manic episode in man, but suggests that an opioid-dopamine interaction may play a pathogenetic role in mania.
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PMID:Sleep deprivation in the rat: an animal model of mania. 877 65


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