UNIPROT:P01189 - FACTA Search

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

A possible dopaminergic regulation of hypothalamic proopiomelanocortin (POMC)-containing neurons has been investigated in rats by means of in vivo and in vitro approaches. Acute or 3-weeks chronic in vivo treatments with the dopaminergic agonists apomorphine (1 mg/kg: s.c.) and 2-Br-alpha-ergocriptine (2.5 mg/kg; s.c.) or the dopaminergic antagonist haloperidol (0.15-3 mg/kg; i.p.) had no significant effect on the concentration of alpha-melanocyte-stimulating hormone (alpha-MSH) in two hypothalamic regions: arcuate nucleus (AN) and dorsolateral area (DLH). In the same way, chronic administration of the dopaminergic agonists or antagonist did not induce any change in hypothalamic contents of beta-endorphin, another peptide derived from POMC. Reverse-phase high-performance liquid chromatographic analysis revealed that acetic acid extracts of AN and DLH both contained two major forms of alpha-MSH-like peptides: deacetylated alpha-MSH and authentic alpha-MSH. The ratio between these two forms was not altered after acute haloperidol treatment (3 mg/kg, i.p.). The possible effect of dopamine on the release of hypothalamic alpha-MSH was studied in vitro using perifused rat hypothalamic slices. Infusion of dopamine (10(-7)-10(-5)M) or its antagonist haloperidol (10(-5)M) had no effect on spontaneous alpha-MSH release from hypothalamic tissue. In addition, none of these drugs had any effect on potassium (50 mM)-induced alpha-MSH release. It is concluded that dopaminergic neurons are not involved in the regulation of synthesis, post-translational processing (acetylation) or release of hypothalamic alpha-MSH.
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PMID:Hypothalamic alpha-melanocyte-stimulating hormone (alpha-MSH) is not under dopaminergic control. 296 Apr 24

The effects of icv administration of beta-endorphin on secretory activity of dopaminergic neurons is described. Homovanillic and dihydroxyphenyl acetic acid levels in cerebrospinal fluid and extracts of brain tissue were determined after administration of beta-endorphin to animals pretreated or not with naloxone. The results suggest that beta-endorphin interferes with formation of dopaminergic metabolites by acting on opioid receptors.
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PMID:Evidence for a role of beta-endorphin in activity of nigrostriatal neurons in the rat. 297 87

From neurointermediate lobe (NIL) extracts of two species of Cyprinidae, Carassius auratus and Cyprinus carpio, several peptides were separated by high-performance liquid chromatography (HPLC) on a C18 muBondapak column eluted with a methanol/acetic acid/triethylamine mixture. Monitoring all fractions by radioimmunoassay (RIA) with an antibody against melanocyte-stimulating hormone (MSH) C terminal gave positive reactions for fractions 7, 11-12, 15-16, 23-24, and 25-27. For further characterization, the elution positions of these peaks were compared to those of known synthetic reference substances. Peak 7 elutes in the same position as oxidized alpha MSH, whereas peak 15-16 matches the elution position of des-acetyl alpha MSH and 23-24 that of alpha MSH. The product from peak 26-27 has several characteristics of the diacetylated form of alpha MSH: its immunoreactivity in RIA, its sensitivity to weak bases and to HCl and its mass spectrum which is identical with that of mammalian diacetyl alpha MSH. In both species, the diacetylated form is predominant in the intracellular pool. This study establishes the coexistence of three different forms of alpha MSH, a des-acetylated, monoacetylated, and diacetylated in the cyprinid NIL extracts.
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PMID:Separation and partial characterization by high-performance liquid chromatography and radioimmunoassay of different forms of melanocyte-stimulating hormone from fish (Cyprinidae) neurointermediate lobes. 298 88

Biotinylated photoaffinity derivatives of adrenocorticotropin (ACTH) are potentially useful tools for the identification of ACTH receptors. The hormone can be attached covalently to its receptor by photoactivation, and the presence of biotin in the molecule facilitates isolation of the solubilized hormone-receptor complex on columns of immobilized succinoylavidin (Suc-avidin). Six photoprobes of ACTH1-24 have been prepared by reacting ACTH1-24, [25-biocytin]ACTH1-25 amide, and [25-dethiobiocytin]ACTH1-25 amide with either 4- or 5-azido-2-nitrophenylsulfenyl (4-NAPS and 5-NAPS, respectively) chlorides in acetic acid. The homogeneity of the photoprobes was carefully monitored by thin-layer chromatography and amino acid analyses of acid hydrolysates. The presence of underivatized starting material in the photoprobes was critically scrutinized by high-pressure liquid chromatography and was estimated to be less than 0.5%. Both the 4- and 5-NAPS derivatives stimulated maximal steroidogenesis (as compared with ACTH1-24) in calf adrenal cortical cells. However, the potencies of the two isomers differed significantly. The ED50 for steroidogenesis with 5-NAPS-ACTH1-24 was 100-fold greater than the standard (ACTH1-24) while that for 4-NAPS-ACTH1-24 was only approximately 7 times greater. Although 4-NAPS-ACTH1-24 was capable of stimulating maximal adenosine cyclic 3',5'-phosphate (cAMP) production, the 5-NAPS derivative was usually not. The level of stimulation with the 5-NAPS derivative varied considerably from cell preparation to cell preparation. ACTH1-24-induced cAMP production was inhibited by 5-NAPS-ACTH1-24 or 5-NAPS-[25-dethiobiocytin]ACTH1-25 amide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthetic tools for adrenocorticotropin receptor identification. 299 May 45

This study was designed to correlate the endocrine responses elicited by acute ether stress with the changes in metabolism of several monoamines in discrete nuclei of the rat brain. Concentrations of norepinephrine (NE), dopamine (DA), and 5-hydroxytryptamine (5-HT) and also of the specific metabolites of NE, DA, and 5-HT, 3-methoxy-4-hydroxyphenylethylene glycol, 3,4-dihydroxyphenylacetic acid, and 5-hydroxyindole-3-acetic acid, respectively, were concurrently measured in microdissected nuclei using high-performance liquid chromatography with electrochemical detection. The ratio of the metabolites to their respective amines was used as an estimate of the metabolism of NE, DA, and 5-HT. Acute exposure to ether vapors induced, within 5-15 min, large increments in plasma levels of adrenocorticotropic hormone (ACTH), beta-endorphin, and prolactin (PRL), and decrements in the levels of plasma growth hormone (GH). Significant increases in NE metabolism were observed in the rostral (ANr) and caudal (ANc) divisions of the arcuate nucleus, as well as in the paraventricular (PVN) and dorsomedial nuclei, 15 min after ether stress. A significant decrease in 5-HT metabolism was observed in the PVN, supraoptic nucleus, and ANc, whereas significant increases in 5-HT metabolism were detected in the suprachiasmatic nucleus and ANr. DA metabolism selectively increased in the ANr. The present results indicate that the acute changes in ACTH, beta-endorphin, PRL, and GH release induced by ether exposure are temporally correlated with increases in NE metabolism in many hypothalamic nuclei; a selective increase in DA metabolism restricted to the ANr, and differential effects on 5-HT metabolism, probably reflecting selective activation or inhibition of different populations of 5-HT neurons.
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PMID:Effect of acute ether stress on monoamine metabolism in median eminence and discrete hypothalamic nuclei of the rat brain and on anterior pituitary hormone secretion. 299 98

Numerous anatomical, pharmacological and electrophysiological data described in the literature indicate that spinal enkephalinergic and serotoninergic systems are probably involved in the control of nociceptive inputs from the periphery to the cerebral cortex. However, reported evidence was generally indirect and did not provide a real demonstration of the physiological participation of these neurones in pain control. This led us to select appropriate experimental approaches for studying directly the activity of spinal enkephalinergic and serotoninergic systems in animals (rat, cat) submitted to noxious stimuli. Owing to two catheters introduced into the subarachnoidal space of anesthetized rats, it was possible to perfuse the whole spinal cord with an artificial cerebro-spinal fluid and thus collect the neuroactive compounds released by spinal neurones (at least those in superficial layers) under various experimental conditions. Using this technique, we observed that some (but not all) nociceptive stimuli such as intense pinching of the muzzle, intraperitoneal injection of acetic acid or noxious heat applied to the muzzle or the tail induced a significant increase in met-enkephalin release from the spinal cord (see fig. 2). Similar effects were observed following the blockade of enkephalin catabolism by thiorphan and bestatin (see fig. 1) indicating that they were not due to some alteration of peptidase activities but really involved the activation of spinal enkephalinergic systems. Since cervical cord transection suppressed the stimulatory action of noxious stimuli on spinal met-enkephalin release, it could be proposed that the mechanisms involved were not limited to the cord but depended on supraspinal structures. Bulbo-mesencephalic serotoninergic neurones projecting to the spinal cord might well correspond to such structures (or at least to some of them) since nociceptive stimuli (such as noxious heat applied to the tail) also evoked a marked increase of serotonin (5-HT) release at the spinal level (fig. 3). Such observations together with indirect evidence reported in the literature suggested therefore that the activation of spinal enkephalinergic systems triggered by noxious stimuli might result from excitatory influence due to descending serotoninergic projections. However, in vitro studies using slices of the dorsal zone of the rat lumbar cord did not reveal any stimulatory effect of 5-HT on the spontaneous or K+-evoked release of met-enkephalin (fig. 4).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The spinal enkephalinergic and serotoninergic systems in the control of transmission of nociceptive messages]. 299 51

Several studies indicate the presence of different pituitary hormones or neuropeptides in ovarian follicular fluid from various species. Recently our group showed that the ovarian follicular fluid of health women contains two of the endogenous opioid peptides, beta-endorphin and methionine enkephalin, in concentrations that are tenfold to twentyfold higher than in circulating plasma. The presence of immunoreactive beta-lipotropin was also shown. The aim of the present study was to evaluate whether adrenocorticotropic hormone, which in pituitary cells is synthesized from proopiomelanocortin such as beta-endorphin and beta-lipotropin, is also present in follicular fluid and the possible changes of proopiomelanocortin-related peptides during the menstrual cycle. Concentrations of beta-endorphin, methionine enkephalin, adrenocorticotropic hormone, and beta-lipotropin were measured in 60 healthy menstruating women at different periods of the menstrual cycle (20 during the follicular, 22 in the preovulatory days, and 18 during the luteal phase). Thirteen women participated in an in vitro fertilization program and thus received clomiphene citrate (100 mg/day from the fifth to the ninth day) plus 5000 IU human chorionic gonadotropin before starting the program. All samples were collected at laparoscopy under general anesthesia. In another eight patients fluid was collected from follicular cysts. Peptides were extracted on octadodecasilyl silica columns with 80% methanol in 0.5 mol/L acetic acid. The identity of follicular fluid beta-endorphin, methionine enkephalin, adrenocorticotropic hormone, and beta-lipotropin and standard peptides was demonstrated with high-pressure liquid chromatography. Peptide concentrations were measured in extracts by radioimmunoassays either directly by (methionine enkephalin and adrenocorticotropic hormone) or after (beta-endorphin and beta-lipotropin) gel filtration on Sephadex G-75. The concentrations of methionine enkephalin, adrenocorticotropic hormone, and beta-lipotropin were similar in the different periods of the cycle. Conversely, beta-endorphin concentrations were significantly higher in preovulatory days than in the other periods; no differences were evident between spontaneous and stimulated cycles. These results indicate that proopiomelanocortin-related peptides are present in the follicular fluid and that beta-endorphin concentrations change during the menstrual cycle, with the highest values occurring in the preovulatory follicle.
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PMID:Proopiomelanocortin-related peptides and methionine enkephalin in human follicular fluid: changes during the menstrual cycle. 303 9

The ontogeny in the rat hypothalamus of arginine vasopressin (AVP) and corticotropin-releasing factor (CRF) was studied to determine whether these two peptides develop in parallel, given the synergistic effect of AVP with CRF on adrenocorticotropic hormone (ACTH) release. Hypothalami and extrahypothalamic cerebrum of 15-day fetal--40-day postpartum rats were extracted in acetic acid for radioimmunoassay. Both AVP- and CRF-like immunoreactivity was detected in whole brain extracts of 15-day fetuses. Hypothalamic CRF levels were low during fetal life, fluctuated around the time of birth, and then progressively rose to 63% of adult levels by day 21 postpartum. Extrahypothalamic levels of brain CRF paralleled hypothalamic levels. Hypothalamic AVP levels began to rise at fetal day 19 in a stepwise manner, with the greatest rise in levels occurring after day 14 postpartum. At day 21 postpartum hypothalamic levels were only 17% of adult. Extrahypothalamic AVP levels initially paralleled those in the hypothalamus but reached a plateau after day 4 post-partum, and did not rise again until after day 21. Hypothalamic CRF and AVP thus do not develop strictly in parallel; the adult ratios of these peptides (approximately 1:40) were never seen during development, perhaps of significance in the observed blunting of the hypothalamic-pituitary-adrenal response to stress in infant rats.
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PMID:Ontogeny of corticotropin-releasing factor and arginine vasopressein in the rat. 326 Sep 99

The analgesic effect of intracerebroventricular administration of morphine, ketocyclazocine, [D-ala2]-methionine enkephalinamide (DAM), [D-ala2-D-leu5]-enkephalin (DADLE), leuenkephalin, metenkephalin, and beta-endorphin on acetic acid-induced abdominal writhing (AAW) was investigated in naive and morphine-tolerant mice. It was found that the relative potencies of a series of opioids are different in naive and morphine-tolerant groups. In naive animals, the order of potency (ED50, nmol) was beta-endorphin greater than morphine = DAM greater than DADLE greater than ketocyclazocine = leuenkephalin = metenkephalin. The morphine-tolerant animals were cross-tolerant to ketocyclazocine and to all the peptides studied; DAM and beta-endorphin exhibited the highest degree of tolerance. In morphine-tolerant animals, the order of potency was morphine = DADLE = beta-endorphin greater than DAM = ketocyclazocine = metenkephalin greater than leuenkephalin. The results indicate that endogenous opioid systems may be affected by tolerance development to morphine.
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PMID:Analgesic cross-tolerance between morphine and opioid peptides. 609 81

The effect of chronic administration of delta 9-tetrahydrocannabinol (delta 9-THC) on the endogenous opiate and catecholamine levels was investigated. Intact male rats were injected daily either with vehicle (50 microliters oil) or delta 9-THC in oil (3 mg delta 9-THC/kg body wt). The treatments were administered subcutaneously over a period of 25 days. All animals were decapitated after the last injection and trunk plasma was assayed for prolactin, beta-endorphin-like immunoreactivity (beta-end LI), norepinephrine (NE), epinephrine (E), dihydroxyphenyl acetic acid (DOPAC) and dopamine (DA). The preoptic area (POA) and medial basal hypothalamus were assayed for methionine enkephalin, beta-endorphin and catecholamines. Chronic delta 9-THC treatment resulted in an increase in POA and MBH methioine-enkephalin and beta-end LI as well as an increase in plasma beta-end LI. The POA, MBH and plasma NE and E levels were lower in these animals when compared with the controls. In the MBH, however, the delta 9-THC treated rats contained higher DA and DOPAC levels when compared with the controls. These results support our view that chronic delta 9-THC administration alters the activities of the endogenous opiate system as well as the catecholaminergic system and consequently impairs the endocrine functions.
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PMID:Effect of chronic administration of delta 9-tetrahydrocannabinol on the endogenous opioid peptide and catecholamine levels in the diencephalon and plasma of the rat. 609 37

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