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 concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary (AP) and the neurointermediate lobe of the pituitary (NIL) was elevated in old as compared to young male rats. Treatment of old male rats with the dopamine precursor, L-DOPA, did not affect the concentration of IR-BE in the AP and produced a significant reduction in the concentration of IR-BE in the NIL. By contrast, administration of the serotonergic neurotoxin, p-CPA, significantly diminished the concentration of IR-BE in the AP of old male rats, while the concentration of IR-BE in the NIL remained unchanged. Hypothalamic IR-BE was decreased in old male rats and was not influenced by administration of L-DOPA or p-CPA. Chromatographic analysis indicated that in the AP of old animals the amount of beta-endorphin relative to beta-lipotropin was increased and was diminished slightly by the treatments. Alterations in IR-BE in the NIL and hypothalamus were represented solely by beta-endorphin. These data suggest that in old male rats, a decrease in dopaminergic activity contributes to the increase in IR-BE levels in the NIL, and an increase in serotonergic function, at least in part, is responsible for the elevation in the level of IR-BE in the AP.
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PMID:The elevation of immunoreactive beta-endorphin in old male rats is related to alterations in dopamine and serotonin. 236 54

Exposure of recently mated female mice to strange male urine revealed that exposure for 8 h was sufficient to produce pregnancy block providing exposure is for two 4-h periods coincident with prolactin surges. Exposure for 8 h between prolactin surges or one 4-h exposure coincident with either the nocturnal or the diurnal prolactin surge was without effect. When bromocriptine, a dopamine agonist, was given coincident with the nocturnal and diurnal prolactin surges, it was equally effective, but the opiate antagonist (naltrexone) administered in a similar manner was without effect. This result indicates that pheromonal action is through excitation of the tuberoinfundibular neurones rather than by inhibition of beta-endorphin neurones. Further evidence for dopamine involvement in pregnancy block is demonstrated by showing DOPA accumulation in the medio-basal hypothalamus following exposure to male urinary pheromones after dihydroxybenzylhydrazine (DHBH) administration, which blocks the enzyme DOPA-decarboxylase. Taken together, this series of experiments provides convincing evidence for the dopamine inhibition of prolactin release being the final pathway for pheromone action in the context of pregnancy block.
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PMID:Restricted exposure of mice to primer pheromones coincident with prolactin surges blocks pregnancy by changing hypothalamic dopamine release. 251 90

To examine the role of monoamines in regulating beta-endorphin levels in discrete brain nuclei, the levels of beta-endorphin-like immunoreactivity (beta-ENDi) were determined in the hypothalamic nuclei of rats 2 h after they were treated with monoaminergic drugs. Sulpiride decreased the levels of beta-ENDi in the nucleus paraventricularis, nucleus arcuatus and median eminence. Domperidone decreased the levels of beta-ENDi in the nucleus aracuatus and median eminence. L-DOPA increased the levels of beta-ENDi in the nucleus anterior hypothalami and median eminence. Phenylephrine or prazosine did not alter the levels of beta-ENDi. Yohimine decreased the levels of beta-ENDI in the nucleus anterior hypothalami. Isoproterenol increased the levels of beta-ENDi in the nucleus arcuatus, and propranolol reversed this effect. These results suggest that dopamine and noradrenaline (via beta-adrenoceptors) may regulate beta-endorphinergic neurons in the rat hypothalamus.
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PMID:Monoaminergic regulation of the levels of beta-endorphin-like immunoreactivity (beta-ENDi) in rat hypothalamic nuclei. 252 3

In humans the major stimulus for cutaneous pigmentation is ultraviolet radiation (UVR). Little is known about the mechanism underlying this response, in part because of the complexity of interactions in whole epidermis. Using a recently developed culture system, human melanocytes were exposed daily to a physiologic range of UVR doses from a solar simulator. Responses were determined 24 hours after the last exposure. There was a dose-related increase in melanin content per cell and uptake of 14C-DOPA, accompanied by growth inhibition. Cells from donors of different racial origin gave proportionately similar increases in melanin, although there were approximately tenfold differences in basal values. Light and electron microscopy revealed UVR-stimulated increases in dendricity as well as melanosome number and degree of melanization, analogous to the well-recognized melanocyte changes following sun exposure of intact skin. Similar responses were seen with Cloudman S91 melanoma cells, although this murine cell line required lower UVR dosages and fewer exposures for maximal stimulation. These data establish that UVR is capable of directly stimulating melanogenesis. Because cyclic AMP elevation has been associated in some settings with increased pigment production by cultured melanocytes, preliminary experiments were conducted to see if the effects of UVR were mediated by cAMP. Both alpha-MSH and isobutylmethylxanthine (IBMX), as positive controls, caused a fourfold increase in cAMP level in human melanocytes and/or S91 cells, but following a dose of UVR sufficient to stimulate pigment production there was no change in cAMP level up to 4 hours after exposure. Thus it appears that the UVR-induced melanogenesis is mediated by cAMP-independent mechanisms.
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PMID:Ultraviolet radiation directly induces pigment production by cultured human melanocytes. 282 34

New syntheses of three thyrotropin releasing hormone (TRH) analogues ([Dopa2]THR, [Nic1]TRH, and [Tyr(30NO2)2]TRH) have been reported (Dopa stands for L-3,4-dihydroxyphenylalanine, Nic--for nicotinic acid and Tyr(3-NO2)--for L-3-nitrotyrosine). These three TRH analogues and five already known ones ([Aad1Tca3]TRH, [D-His2]TRH, [D-Pro3]TRH, [Pro-NH-NH2(3)]TRH and [Tyr2]TRH), were studied in vitro for their binding activity to rat pituitary TRH receptors and a-MSH releasing activity in the neuro-intermediate lobe of frogs. Competition of analogues for 3H-TRH binding to rat anterior pituitary membrane fraction was used. One of ten tested analogues ([Aad1, Tca]3 TRH) was as potent as TRH in competing for high-affinity binding sites (Kd = 8.5 nM). The binding activity of diastereoisomers ([D-His2]TRH and [D-Pro3]TRH) was reduced as well as that of analogue [Pro-NH-NH2(3)]TRH. The rest of the analogues were inactive. The binding activities were in good accordance with alpha-MSH releasing activities.
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PMID:Synthesis, receptor binding affinities and alpha-MSH releasing activities of TRH analogues. 299 54

Brain enkephalin receptors were studied in post-mortem brain samples of 27 patients with Parkinson's disease and of 26 control subjects without extrapyramidal disorders by the radioligand-binding technique using 3H-leu-enkephalin, 3H-met-enkephalin and 3H-naloxone. The specific binding of both 3H-leu- and 3H-met-enkephalins was significantly increased in the caudate nucleus, putamen, nucleus accumbens, limbic cortex and hippocampus. Scatchard analysis showed that there was an increase in the receptor number, but no significant changes in the mean dissociation constant. Levodopa treatment did not have any significant effect on the enkephalin bindings. A significantly decreased binding of 3H-naloxone was found in the parkinsonian caudate nucleus. Thus there is a supersensitivity of a population of enkephalin receptors in the striatum and limbic system, as well as a loss of other opiate receptors in the striatum, suggesting the involvement of certain brain enkephalin neurons in the pathophysiological process of Parkinson's disease.
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PMID:Brain enkephalin receptors in Parkinson's disease. 632 47

Deep brain stimulation (thalamic relay nucleus, periaqueductal gray and internal capsule) was applied to various cases of intractable pain, and the resulting degree of pain reduction and alteration in beta-endorphin immunoreactivity in the cerebrospinal fluid (CSF) were compared. The following results were obtained. (1) The studies on intractable pain revealed that the levels of beta-endorphin immunoreactivity in the CSF were lower than those in the control group. (2) Thalamic relay nucleus stimulation proved effective not only for deafferentiation pain, but also for somatogenic pain. No relationship was, however, noted between pain reduction and the rate of increase of beta-endorphin immunoreactivity in the CSF. (3) The incidence of stimulation tolerance following prolonged stimulation of the thalamic relay nucleus can be reduced to a minimum by administration of L-DOPA. It is concluded that the increase in beta-endorphin in the CSF is not the direct and major cause of pain reduction during treatment by thalamic relay nucleus stimulation. It may be assumed that neuronal facilitation on the monoaminergic descending pain inhibitory system plays a role in reducing pain.
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PMID:Thalamic relay nucleus stimulation for relief of intractable pain. Clinical results and beta-endorphin immunoreactivity in the cerebrospinal fluid. 632 55

Administration of glucocorticoids decreases the release of corticotropin-releasing hormone and in vitro turnover of norepinephrine (NE) in the paraventricular nucleus (PVN) of the hypothalamus, and immobilization (IMMO) markedly increases NE release and stimulates corticotropin-releasing hormone neurons in the PVN. This study assessed whether hypercortisolemia affects in vivo indexes of catecholaminergic activation in the PVN. Microdialysis was used to simultaneously measure PVN microdialysate concentrations of NE, the neuronal NE metabolite dihydroxyphenylglycol, the extraneuronal NE metabolite methoxyhydroxyphenylglycol, and the dopamine metabolite dihydroxyphenylacetic acid before, during, and after 2 h of IMMO. Catecholamine synthesis was examined based on elevations of 3,4-dihydroxyphenylalanine levels after local perfusion with NSD-1015, an inhibitor of L-aromatic acid decarboxylase. Cortisol (CORT; 25 mg/kg.day) or vehicle (VEH; saline) was infused sc for 7 days via an osmotic minipump. CORT-treated rats had lower basal NE, dihydroxyphenylglycol, methoxyhydroxyphenylglycol, and dihydroxyphenylacetic acid levels and significantly smaller levels of all these compounds during IMMO than VEH-treated rats. CORT-treated rats also had less NSD-1015-induced accumulation of microdialysate 3,4-dihydroxyphenylalanine at baseline and during IMMO than VEH-treated rats. Basal and IMMO-induced plasma ACTH and corticosterone responses were reduced in CORT-treated rats. The results indicate that chronic hypercortisolemia decreases basal levels and stress-induced increments in indexes of release, metabolism, turnover, and synthesis of catecholamines in the PVN and suggest that glucocorticoids restrain the limit of hypothalamo-pituitary-adrenocortical axis activation during stress by attenuating catecholamine synthesis and release in the PVN.
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PMID:Catecholaminergic inhibition by hypercortisolemia in the paraventricular nucleus of conscious rats. 758 11

The endogenous pentapeptides, met-enkephalin and leuenkephalin, similar to their parent structures, beta-endorphin or dynorphin, bind to opioid receptors of the nociceptive system thus provoking analgesic responses. Peroxidases and phenolases (tyrosinase, catecholase) were shown to dimerize these pentapeptides thus possibly modulating their activity and/or lifetime. Extracts from plants from the order of the Papaverales contain isoquinoline alkaloids. Since the benzoisoquinolines are known to possess sedative-hypnotic activities, the potential effects of extracts from two species from this plant group, Eschscholtzia californica (Papaveraceae) and tyrosinase-catalyzed dimerization and/or oxidation of met-enkephalin were investigated. The results of the study show that the peroxidase-catalyzed dimerization via the tyr-residues is especially inhibited by the C. cava extract. The tyrosinase-catalyzed reaction yields five different products A-E, according to their HPLC-retention times. Consisting of the 4:1 (v/v) combination of the extracts from E. californica and C. cava, Phytonoxon N (abbreviated as PN) stimulates the formation of minor products A, B and E, whereas the formation of the major products C and D is inhibited. Only products C and D exhibit properties similar to the peroxidase-derived dimer. Product A is likely to be identical to DOPA-enkephalin.
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PMID:Effects of ethanolic extracts from Eschscholtzia californica and Corydalis cava on dimerization and oxidation of enkephalins. 771 Apr 33

We used the met-enkephalin analog (D-Met2,Pro5)-enkephalinamide (DMPEA) to investigate enkephalinergic control of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion. Systemic (s.c.) administration of DMPEA elevated plasma titers of alpha-MSH in a dose- and time-related manner. Pretreatment with the opiate antagonist naltrexone had no effect on basal plasma levels of alpha-MSH but blocked DMPEA-induced alpha-MSH release. Treatment with a dose of naltrexone sufficient to block DMPEA-induced secretion of alpha-MSH had no effect on stress-induced secretion of alpha-MSH. Although pretreatment with the dopamine receptor agonist apomorphine prevented DMPEA-induced alpha-MSH secretion, DMPEA had no effect on the synthetic activity of tuberohypophysial dopamine neurons as gauged by measuring the accumulation of 3,4-dihydroxyphenylalanine in the neurointermediate lobe (NIL) following administration of NSD-1015. In vitro treatment of isolated NILs with DMPEA resulted in a significant increase in alpha-MSH release. Naltrexone completely blocked the stimulatory effects of DMPEA on alpha-MSH release in vitro. Our results indicate that DMPEA stimulates alpha-MSH secretion by acting directly through opiate receptors at the level of the NIL.
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PMID:Effects of the enkephalin analog (D-Met2,Pro5)-enkephalinamide on alpha-melanocyte-stimulating hormone secretion. 823


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