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)

In an attempt to clarify whether m-chlorophenylpiperazine-(m-CPP) and 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane-(DOI) induced increases in plasma adrenocorticotropin hormone, corticosterone and prolactin secretion are mediated by the same or different mechanisms, we studied the time course of development of tolerance to the neuroendocrine effects of m-CPP (2.5 mg/kg/day) and DOI (2.5 mg/kg/day) in rats and, furthermore, also evaluated possible cross-tolerance in responses to m-CPP and DOI. We observed the development of tolerance in adrenocorticotropin hormone responses after a single i.p. injection of m-CPP. However, there was no cross-tolerance to DOI when chronic (13 days) m-CPP-treated animals were challenged with DOI (2.5 mg/kg). Injections of DOI (2.5 mg/kg) for six days were required before tolerance developed to the effect of DOI on adrenocorticotropin hormone. Furthermore, cross-tolerance was observed when DOI-treated animals (2.5 mg/kg/day x 6) were challenged with m-CPP (2.5 mg/kg) on day 7. In contrast, daily administration of m-CPP and DOI for 13 days did not produce tolerance to their stimulating effects on corticosterone and prolactin secretion. Hypothalamic levels of 5-hydroxyindoleacetic acid but not 5-HT were significantly reduced after acute or subchronic administration of both m-CPP and DOI. Furthermore, no change in the approximate 50% reduction in 5-hydroxyindoleacetic acid after m-CPP was observed after subchronic administration of this drug. These findings suggest that separate mechanisms mediate m-CPP and DOI-induced adrenocorticotropin hormone secretion in rats.
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PMID:Repeated administration of meta-chlorophenylpiperazine or 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane produces tolerance to its stimulatory effect on adrenocorticotropin hormone but not prolactin or corticosterone secretion in rats. 893 Jan 84

To obtain information on long-term circadian consequences of administering melatonin neonatally to rats, we assessed the 24-hour rhythms of 1) serum prolactin (PRL), luteinizing hormone (LH), and growth hormone (GH), and 2) medial basal hypothalamic dopamine (DA) and serotonin (5-HT) metabolism and corticotropin-releasing hormone (CRH) content in 60-day old male rats injected with 100 micrograms of melatonin on the 5th day of life. Controls receiving vehicle alone showed serum PRL concentration (when 60 days of age) attaining its maximum at the end of the light period (i.e., at 2000 hr), while in melatonin-injected rats high PRL values were found between 1200 and 2000 hr. Twenty-four hour changes in serum LH levels exhibited a maximum at noon, and to a similar extent in vehicle- and melatonin-treated rats. Neonatal melatonin injection did not affect serum GH concentration when the rats were adult. In the medial basal hypothalamus (MBH), the dihydroxyphenyl acetic acid (DOPAC)/ DA ratio attained a maximum at midnight, its amplitude being significantly higher in melatonin- than in vehicle-treated rats. Neonatally melatonin-injected rats also exhibited a second maximum in DOPAC/DA ratio at noon, coinciding with a minimum in DA levels of MBH. The 5-hydroxyindoleacetic acid (5-HIAA)/5-HT ratio in MBH showed significant diurnal variations in vehicle-injected controls with maxima at 1200 and 0400 hr, while in melatonin-treated rats a single maximum occurred at 2400 hr. These maximum correlated with minima in 5-HT content of MBH. Neonatal melatonin injection brought about a significant increase in the CRH content of MBH, as well as distortion of its diurnal rhythmicity, a maximum being found at noon in controls and at 1800 hr in melatonin-treated rats. The results indicate that exposure to melatonin early in life affects subsequent diurnal rhythmicity of PRL release, and of DA and 5-HT turnover and CRH content in the MBH of rats.
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PMID:Twenty-four hour rhythms of serum prolactin, growth hormone and luteinizing hormone levels, and of medial basal hypothalamic corticotropin-releasing hormone levels and dopamine and serotonin metabolism in rats neonatally administered melatonin. 906 71

Agonistic behavior, brain concentrations of serotonin (5-hydroxytryptamine, 5-HT), and 5-hydroxyindoleacetic acid (5-HIAA, the main 5-HT metabolite), plasma cortisol levels, and the pituitary expression of pro-opiomelanocortin (POMC) A and B mRNA were determined in socially dominant and subordinate rainbow trout after 1 or 7 days of social interaction. Telencephalic and brain stem 5-HIAA/5-HT ratios, plasma cortisol levels, and pituitary POMC mRNA concentrations were elevated in fish being subordinate for 1 day. Furthermore, neither telencephalic 5-HIAA/5-HT ratios nor pituitary POMC A or POMC B mRNA expression showed any decline after 7 days of social interaction. By contrast, plasma cortisol concentrations of subordinate fish declined after 7 days but were still significantly higher than in dominant fish. Furthermore, in subordinate fish, hypothalamic 5-HIAA/5-HT ratios and plasma cortisol levels were highly correlated, suggesting an important role of hypothalamic 5-HT in the regulation of the teleost hypothalamic-pituitary-interrenal (HPI) axis. The number of aggressive acts received and plasma cortisol levels were highly correlated in 1-day subordinates, a relationship not seen in fish subjected to 1 wk of subordination. Thus the chronic stress experienced by subordinates in established dominance hierarchies appears to be more closely related to the threat imposed by the presence of the dominant fish than to actual aggressive encounters. The sustained elevation of pituitary POMC mRNA expression, an effect mainly related to an increase of melanotropic POMC expression, in subordinates could be a mechanism serving to maintain HPI axis excitability and promote acclimation in these individuals.
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PMID:Elevation of brain 5-HT activity, POMC expression, and plasma cortisol in socially subordinate rainbow trout. 953 Feb 29

Children with the opsoclonus-myoclonus syndrome (OMS) usually respond to corticotropin (adrenocorticotrophic hormone, ACTH) treatment but the mechanism of benefit is unknown. We previously showed that both cerebrospinal fluid (CSF) homovanillic acid (HVA) and 5-hydroxyindole-acetic acid (5-HIAA) concentrations are low in pediatric OMS. In this study, we measured levels of CSF Dopa, catecholamines, deaminated metabolites of catecholamines, as well as HVA and 5-HIAA in eight patients before and during treatment with ACTH. All the children were ACTH-responsive with 50-70% improvement in multiple clinical features of OMS. ACTH treatment reduced the HVA concentration in every child by a mean of 21% (p < 0.001). Treatment with ACTH was associated with significant correlations between dopaminergic markers such as HVA, dihydroxyphenylacetic acid (DOPAC), and Dopa. There were no significant changes in the CSF concentrations of the noradrenergic markers norepinephrine (NE) and dihydroxyphenylglycol (DHPG), or the serotonergic marker 5-HIAA. The only child with a marked inflammatory pattern in CSF, which was reversed by ACTH, was atypical for a large increase in NE and decrease in 5-HIAA during ACTH treatment. Beneficial effects of ACTH in OMS are not associated with normalization of HVA or 5-HIAA levels. The pattern of decreased HVA and unchanged DOPAC levels could reflect decreased extraneuronal uptake of catecholamines (which steroids inhibit) or decreased 0-methylation of catecholamines in nonneuronal cells.
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PMID:Monoaminergic effects of high-dose corticotropin in corticotropin-responsive pediatric opsoclonus-myoclonus. 961 46

Eight multiparous non-lactating pregnant Holstein cows at 198 +/- 35 d of gestation, weighing 608 +/- 24 kg, were confined to wooden metabolic cages in an electric and magnetic field chamber with a 12:12 h light:dark cycle. Subarachnoidal catheters were installed 5 d before the activation of the electric and magnetic fields. The cows were exposed to electric and magnetic fields (60 Hz, 10 kV/m and 30 microT) continuously except for the feeding and cleaning time for an average of 21.44 +/- 1.4 h per day for a period of 30 d. Cerebrospinal fluid samples were collected on three consecutive days before an exposure period of 30 d, on the last 3 d of the exposure period, and for 3 d starting 5 d after the exposure period. The concentrations of beta-endorphin, tryptophan, 5-hydroxyindoleacetic acid, homovanillic acid, 3-methoxy-4-hydroxyphenylethyleneglycol and quinolinic acid in cerebrospinal fluid were determined. There was a significant increase in quinolinic acid, and a trend towards an increase in tryptophan, findings consistent with a weakening of the blood-brain barrier due to exposure to the electric and magnetic fields.
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PMID:Effects of electromagnetic fields on the levels of biogenic amine metabolites, quinolinic acid, and beta-endorphin in the cerebrospinal fluid of dairy cows. 982 Nov 57

High-frequency electrical stimulations of thalamic nuclei are currently used for the suppression of parkinsonian or essential tremor and for the relief of some types of intractable pain in man. However, the mechanisms by which such stimulations exert their therapeutic effects are essentially unknown. Attempts were made to provide some insight into these mechanisms by measuring the levels of the dopamine metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and met-enkephalin-like immunoreactivity in ventricular cerebrospinal fluid (CSF) of patients with Parkinson's disease (PD) or multiple sclerosis (MS) after a 30-minute therapeutic electrical stimulation of the ventralis intermedius nucleus of the thalamus. In nonstimulated control patients, the levels of these compounds did not significantly differ in two CSF samples taken 30 minutes apart. In stimulated patients, a decrease in dopamine metabolite levels associated with a relative increase in met-enkephalin-like immunoreactivity were observed in the CSF sample taken after the 30-minute stimulation as compared to the sample taken immediately before the stimulation. In contrast, the levels of 5-HIAA remained unaffected by the stimulation. These data confirmed the existence of negative interactions between dopaminergic and enkephalinergic systems in man similar to those previously demonstrated in rats. In addition, they suggest that alterations in dopaminergic or enkephalinergic neurotransmission might be involved in the therapeutic action of thalamic electrical stimulation in patients with parkinsonian symptoms and other patients.
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PMID:Opposite changes in dopamine metabolites and met-enkephalin levels in the ventricular CSF of patients subjected to thalamic electrical stimulation. 1044 54

A 57-year-old man with a history of hepatic adenocarcinoma was referred 3 years after his diagnosis with a choroidal tumor in the right eye. Results of a transscleral excision biopsy revealed the tumor to be an amyloid-rich neuroendocrine metastasis. The patient subsequently developed cushingoid features and investigations revealed ectopic corticotropin syndrome, an elevated urinary 5-hydroxyindoleacetic acid level, and neuroendocrine metastasis in several locations. The choroidal neuroendocrine metastasis stained negative for serotonin and corticotropin. The source of the ectopic corticotropin and the location of the primary tumor have not been found. This case demonstrates that disseminated neuroendocrine tumors may rarely cause ocular lesions before systemic endocrine sequelae arise.
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PMID:A choroidal amyloid-rich neuroendocrine tumor: initial manifestation of Cushing syndrome. 1044 55

Transgenic (TG) mice deficient in glucocorticoid receptors (GR) were used in order to study the effects of a reduced GR function on adrenocorticotropin hormone and corticosterone plasma levels and on serotonin metabolism in different brain areas under basal resting conditions, after a 30-min restraint stress and 60 min after the end of the restraint stress. There was no difference in basal or stress-induced levels of either adrenocorticotropin hormone or corticosterone in control and TG mice, but the return of adrenocorticotropin hormone to basal values after the end of the stress was delayed in TG mice. Under basal conditions, the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine was decreased only in the hippocampus of TG mice compared to controls. In the brain stem, the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine increased compared to basal values after a 30-min restraint stress and values were still high 60 min after the end of the restraint stress in both control and TG mice. In the hippocampus, the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine increased at the end of the stress and returned to basal levels 60 min later in control mice, whereas there was no change at the end of the stress but an increase 60 min later in TG mice. Finally there was no change in serotonin metabolism in the cortex, striatum or hypothalamus in either group or situation. Our results support the hypothesis of a tonic activation of serotonin turnover by corticosterone through GR in the mouse hippocampus. Moreover, stress-induced stimulation of serotonin metabolism in the brain stem and hippocampus appears to be delayed in TG mice compared to control mice. These results are particularly relevant for mood disorders such as depression where alterations of serotoninergic transmission might be secondary to an impairment of GR functions.
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PMID:Regional serotonin metabolism under basal and restraint stress conditions in the brain of transgenic mice with impaired glucocorticoid receptor function. 1065 34

Arctic charr were allowed to interact in groups of three for 5 days. Skin darkness was quantified by measuring the mean brightness of individual fish before and after social interaction. Brain levels of monoamines and monoamine metabolites and plasma concentrations of cortisol, adrenocorticotropic hormone (ACTH), N-acetyl-(beta)-endorphin and alpha-melanocyte-stimulating hormone (alpha-MSH) were analysed. The results show that social subordination resulted in a significant skin darkening. Furthermore, plasma concentrations of alpha-MSH, ACTH and cortisol were elevated in subordinates, and these fish also displayed elevated levels of 5-hydroxyindoleacetic acid (5-HIAA) in the telencephalon. The ratio of [5-HIAA] to serotonin [5-HT] was increased in several brain areas. In addition, the ratio of 3-methoxy-4-hydroxyphenylglycol (MHPG) to norepinephrine (NE) concentrations was significantly increased in the optic tectum of subordinate fish. Skin darkness following social interaction showed a significant positive correlation with plasma levels of alpha-MSH. Plasma levels of ACTH and alpha-MSH were both positively correlated with that of cortisol. Brain [5-HIAA]/[5-HT] ratios were positively correlated with circulating plasma levels of ACTH, and a similar positive correlation was seen between [MHPG]/[NE] ratios in the optic tectum and plasma levels of ACTH, alpha-MSH and N-acetyl-beta-endorphin. In contrast, hypothalamic [MHPG]/[NE] ratios displayed a negative correlation with plasma alpha-MSH concentrations. The present study demonstrates that social stress induces skin darkening in Arctic charr and that this effect could be mediated by a stress-induced increase in the levels of alpha-MSH in the circulation. Furthermore, the results suggest that 5-HT and NE in the central nervous system could be factors regulating the pituitary release of ACTH and alpha-MSH.
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PMID:Skin darkening, a potential social signal in subordinate arctic charr (Salvelinus alpinus): the regulatory role of brain monoamines and pro-opiomelanocortin-derived peptides. 1080 61

Corticotropin-releasing hormone plays an important role in the coordination of various responses to stress. Previous research has implicated both corticotropin-releasing hormone and the serotonergic system as causative factors in the development and course of stress-related psychiatric disorders such as major depression. To delineate the role of the corticotropin-releasing hormone receptor type 1 (CRH-R1) in the interactions between corticotropin-releasing hormone and serotonergic neurotransmission, in vivo microdialysis was performed in CRH-R1-deficient mice under basal (home cage) and stress (forced swimming) conditions. Hippocampal dialysates were used to measure extracellular levels of serotonin and its metabolite 5-hydroxyindoleacetic acid, and free corticosterone levels to monitor the status of the hypothalamic-pituitary-adrenocortical axis. Moreover, behavioural activity was assessed by visual observation and a scoring paradigm. Both wild-type and heterozygous mutant mice showed a clear diurnal rhythm in free corticosterone. Free corticosterone concentrations were, however, lower in heterozygous mutant mice than in wild-type animals and undetectable in homozygous CRH-R1-deficient mice. Homozygous CRH-R1-deficient mice showed enhanced hippocampal levels of 5-hydroxyindoleacetic acid but not of serotonin during the light and the dark phase of the diurnal cycle, which may point to an enhanced synthesis of serotonin in the raphe-hippocampal system. Moreover, the mutation resulted in higher behavioural activity in the home cage during the light but not during the dark period. Forced swimming caused a rise in hippocampal serotonin followed by a further increase after the end of the stress paradigm in all genotypes. Homozygous and heterozygous mutant mice showed, however, a significantly amplified serotonin response to the forced swimming as compared to wild-type control animals. We conclude that CRH-R1-deficiency results in reduced hypothalamic-pituitary-adrenocortical axis activity, in enhanced synthesis of serotonin during basal conditions, and in an augmented response in extracellular levels of serotonin to stress. These data provide further evidence for the intricate relationship between corticotropin-releasing hormone and serotonin and the important role of the CRH-R1 herein.
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PMID:Corticotropin-releasing hormone receptor type 1-deficiency enhances hippocampal serotonergic neurotransmission: an in vivo microdialysis study in mutant mice. 1180 62


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