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)

A radioimmunoassay is described for the measurement of alpha-melanocyte-stimulating hormone (alpha-MSH). The antibody was produced in rabbits by immunization with alpha-MSH coupled to bovine serum albumin with carbodiimide. The antibody did not react significantly with ACTH, beta-MSH, or 6 fragments of ACTH. The sensitivity and reliability of the assay were improved by employing a simple plasma extraction procedure. When applied to a 2 ml plasma sample, the detection limit of the radioimmunoassay was 6 pg/ml. ACTH was measured with a sensitive and specific radioimmunoassay previously described for humans and adapted for the rat. The anti-ACTH serum cross-reacted with the biologically active portion of alpha-p ACTH and not with alpha-MSH, beta-MSH or the alpha-p 17-39 and alpha-p 25-39 fragments of ACTH. The detection limit was 20 pg/ml. Plasma and pituitary alpha-MSH and ACTH had the same immunoreactivity as synthetic alpha-MSH and ACTH. alpha-MSH and ACTH contents of the rat neurointermediate lobe were 1398 +/- 360 (SE) ng and 28.2 +/- 2.9 ng, respectively, while in the anterior lobe they were 102 +/- 31 ng and 551 +/- 36 ng, respectively. The plasma alpha-MSH concentration at 8 AM in male rats was 64 +/- 8 pg/ml when the plasma ACTH concentration was 92 +/- 15 pg/ml. Over a 24-hour period two peaks of plasma alpha-MSH were observed, one at 4 AM (142 +/- 35 pg/ml) and the other at 4 PM (139 +/- 26 pg/ml). Plasma ACTH was higher at noon (151 +/- 43 pg/ml) and 4 PM (130 +/- 48 pg/ml). Short-term exposure to ether induced a transient increase in alpha-MSH level 5 min later and a rapid return to normal levels. Plasma ACTH increased significantly 2.5 min after the onset of ether stress and remained high for 30 min. Two hours' exposure to ether did not change plasma alpha-MSH, although a 3-fold increase in plasma ACTH was observed. Haloperidol injection was followed by a large increase in plasma alpha-MSH, whereas ACTH levels increased similarly after saline and Haloperidol injection. Corticoid administration reduced ACTH, but not alpha-MSH. Three weeks after adrenalectomy, alpha-MSH levels had not changed but ACTH levels had increased ten-fold. These data indicate that alpha-MSH is secreted in the rat, and that the regulation of its secretion is different from that of ACTH.
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PMID:Immunoreactive alpha-MSH and ACTH levels in rat plasma and pituitary. 17 89

A modification of our previous radioimmunoassay (RIA) for alpha-melanocyte-stimulating hormone (alpha-MSH) is described that permits the measurement of circulating levels in the rat without the need for an extraction procedure. Using this method, serum and neurointermediate lobe (NIL) immunoreactive alpha-MSH levels were measured in rats after administration of haloperidol, 2-bromo alpha-ergocryptine (CB 154), and alpha-methyl-p-tyrosine (alpha-MPT). Haloperidol caused a rapid increase, alpha-MPT a slow increase, and CB 154 a rapid decrease in serum alpha-MSH. At the time intervals studied none of the drugs had any significant effect on NIL alpha-MSH content. It was concluded from the results of the above drug treatments that modulation of dopaminergic neurotransmission both pre- and postsynaptically produces changes in serum immunoreactive alpha-MSH levels. This supports the suggestion that circulating alpha-MSH in the rat is under an inhibitory control by a catecholaminergic system.
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PMID:An improved radioimmunoassay for alpha-melanocyte-stimulating hormone (alpha-MSH) in the rat: serum and pituitary alpha-MSH levels after drugs which modify catecholaminergic neurotransmission. 20 51

The effect of excitatory amino acid receptor antagonists, (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5, 10-imine hydrogen maleate ((+)-MK-801), (+/-)-3-(2-carboxy-piperazin-4-yl)-propyl-1-phosphonic acid (CPP), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (+/-)-2-amino-4-phosphonobutanoic acid (AP-4), on penile erection and yawning induced by subcutaneous apomorphine (80 micrograms/kg), intracerebroventricular (i.c.v.) oxytocin (30 ng) and adrenocorticotropin (ACTH)-(1-24) (10 micrograms) was studied in male rats. Intraperitoneal (0.1-0.4 mg/kg) and i.c.v. (10-50 micrograms) (+)-MK-801 prevented dose dependently the penile erection and yawning induced by the three drugs. The (+)-MK-801 effect coincided with the appearance of head weaving, body rolling, hyperlocomotion and ataxia. Haloperidol (0.5 mg/kg i.p.) antagonized the prevention by (+)-MK-801 of oxytocin responses. Penile erection but not yawning was also prevented by high, but not low doses of CPP and CNQX, which impaired motor performance, AP-4 was ineffective at all doses tested. The above compounds were ineffective when injected into the paraventricular nucleus of the hypothalamus, the brain area where apomorphine and oxytocin act to induce penile erection and yawning. The results suggest that excitatory amino acid transmission is not involved in the expression of penile erection and yawning induced by the above compounds.
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PMID:Effect of excitatory amino acid receptor antagonists on apomorphine-, oxytocin- and ACTH-induced penile erection and yawning in male rats. 135 47

A possible catecholaminergic regulation of hypothalamic alpha-melanocyte-stimulating hormone (alpha-MSH) has been investigated in male rats by an in vivo approach. The hormone was measured by radioimmunoassay in three hypothalamic regions: medial basal hypothalamus, preoptic hypothalamic area and dorsolateral hypothalamus. The tyrosine hydroxylase inhibitor alpha-methyl-para-tyrosine (300mg/kg) increased the hypothalamic alpha-MSH content in medial basal hypothalamus and preoptic hypothalamic area when it was measured at 22:00 h. Diethyldithiocarbamate (600mg/kg), which inhibits dopamine beta-hydroxylase, as well as 2-3-dichloromethylbenzylamide (25mg/kg), which acts on the phenylethanolamine-NCH3 transferase also increased the alpha-MSH content in the above mentioned discrete areas. The alpha-adrenoceptor antagonist phenoxybenzamine (15mg/kg), as well as the alpha 1-adrenoceptor antagonist prazosin (1.0mg/kg), also increased the hypothalamic alpha-MSH content in medial basal hypothalamus and preoptic hypothalamic area. None of these agents modified alpha-MSH content in dorsolateral hypothalamus. Haloperidol (1.2mg/kg), a dopaminergic receptor antagonist, propranolol (6.0mg/kg) and yohimbine (10mg/kg) (non selective beta- and alpha 2-adrenergic antagonist drugs respectively) had no effect on the alpha-MSH in any of the hypothalamic areas studied. These results indicate that the catecholaminergic system is involved in the control of proopiomelanocortin derived hypothalamic alpha-MSH through an alpha 1-adrenoreceptor. The data suggest that the control mechanism in the two alpha-MSH hypothalamic pools are different.
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PMID:Evidence for catecholaminergic control of alpha-melanotropin (alpha-MSH) content in hypothalamic areas. 136 45

The effects of single and repeated doses of met-enkephalin (Met-E) on the ultrastructure and TSH-like immunoreactivity (IR) of pituitary TSH-producing cells, and TSH plasma levels in male rats and the influence of pretreatment with a dopamine antagonist, haloperidol, on these, were evaluated. Both acute and repeated Met-E administration produced changes in TSH cells consisting of: an increase in TSH-like IR, enlargement and dilation of RER and Golgi apparatus, size-increase of secretory granules, and the presence of a variable number of cytoplasmic vacuoles. The ultrastructural changes were more evident in the chronically treated animals, whereas no differences were found in IR-intensity between both Met-E treated groups. Haloperidol alone modifies neither ultrastructure nor TSH-like IR of TSH producing cells, but it prevented the Met-E produced changes. On the other hand, Met-E treatment resulted in a decrease of TSH plasma levels, but being significant only in the acutely injected animals. No variations were produced by haloperidol alone, but it prevented the decrease of TSH plasma levels stimulated by Met-E. Our results suggest that Met-E plays a role in the release of TSH, and that dopamine is implicated in this process. The possible mechanisms through which Met-E influences TSH secretion are discussed.
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PMID:Study of the rat TSH-producing cells after met-enkephalin treatment: effects of dopamine antagonists. 176 27

Beagle dogs were given saline, insulin or the dopamine antagonist, haloperidol, to examine peripheral concentrations of immunoreactive (ir)-pro-opiomelanocortin (POMC) peptides resulting from pars distalis or pars intermedia stimulation. Six beagles were given each test substance on separate occasions with and without dexamethasone pretreatment. Plasma was assayed directly for glucose, ir-ACTH, ir-alpha-MSH, cortisol and, after Sephadex G-50 Fine gel filtration chromatography, for ir-beta-lipotrophin (ir-beta-LPH) and ir-beta-endorphin (ir-beta-END) content. Injection of 0.5 units insulin/kg lowered (P less than 0.01) plasma glucose from 4.9 +/- 0.3 mmol/l (mean +/- S.D., saline controls) to 2.3 +/- 0.5 mmol/l, coincident with increasing ir-ACTH (9.5 +/- 3.1 to 106 +/- 54 pmol/l), cortisol (52 +/- 27 to 221 +/- 27 nmol/l), ir-beta-LPH (not detectable to 34 +/- 18 pmol/l) and ir-beta-END (not detectable to 52 +/- 22 pmol/l). Plasma ir-alpha-MSH concentrations were not affected by insulin. Pretreatment with dexamethasone abolished the ir-ACTH, cortisol, ir-beta-LPH and ir-beta-END increases in response to 0.75 units insulin/kg. Haloperidol (1 mg/kg) increased (P less than 0.01) plasma ir-ACTH (to 103 +/- 63 pmol/l), cortisol (to 243 +/- 11 nmol/l), ir-beta-LPH (to 16 +/- 6 pmol/l), ir-beta-END (to 136 +/- 73 pmol/l) and additionally raised ir-alpha-MSH (7 +/- 8 pmol/l in saline controls to 131 +/- 80 pmol/l after haloperidol).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential secretion of pro-opiomelanocortin peptides by the pars distalis and pars intermedia of beagle dogs. 283 53

The effects of short- and long-term neuroleptic therapy on peripheral secretion of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) were examined in 25 chronic schizophrenic patients. Haloperidol was given to 8 patients for 10 days (group A: 0.1 mg/kg b.w./day) and to another group of 8 patients for 30 days (group B: 10-18 mg/day). The other 9 patients were given a combination of haloperidol (6-30 mg/day) with either chlorpromazine (25-75 mg/day), clotiapine (40-60 mg/day), or fluphenazine decanoate (25-75 mg/month) for 14-18 months (group C). beta-EP and beta-LPH levels were assayed before and after each treatment. Haloperidol plasma levels were assayed in group B patients at the end of treatment. beta-EP mean basal levels were higher in patients than in controls; however, beta-LPH mean basal levels were higher only for group A patients. After treatment, the mean levels did not differ from those prior to therapy in groups A and B, while beta-LPH levels were significantly higher in group C. Level increases or decreases in single patients did not correlate with drug dose or duration of treatment, with baseline peptide levels or with the clinical effects of the various treatments.
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PMID:Effects of neuroleptic treatments on peripheral opioid secretion. 289 44

Proopiomelanocortin (POMC) is posttranslationally processed in the intermediate lobe of the pituitary to both N-terminally acetylated and nonacetylated forms of alpha MSH and beta-endorphin (beta END). N-Acetylation substantially modifies the physiological responses produced by both peptides, suggesting that the activity of the peptide acetyltransferase, which posttranslationally acetylates beta END and des-acetyl-alpha MSH, may play an important role in defining the biological activity of the secretory products of the intermediate pituitary lobe. The present results demonstrate that peptide acetyltransferase activity is induced by treating rats chronically with the dopamine receptor antagonist haloperidol. Haloperidol administration produced parallel and essentially equivalent increases in acetyltransferase activity, POMC mRNA levels, and the content and secretion of POMC-derived peptides in the neurointermediate pituitary. Time-course and dose-response studies further demonstrated that acetyltransferase activity covaried with POMC mRNA and peptide levels. Chronic treatment with the dopamine receptor agonist bromocriptine had the opposite effects; it lowered acetyltransferase activity, POMC mRNA levels, and alpha MSH and beta END immunoreactivities. Subcellular fractionation showed that acetyltransferase activity was localized in three subcellular compartments corresponding in density to secretory vesicles, rough endoplasmic reticulum and Golgi apparatus, and cytosol. Haloperidol treatment significantly increased the specific activity of the secretory vesicle-associated acetyltransferase without affecting the specific activity of the enzymes present in the endoplasmic reticulum or cytosol. Together, these data indicate that peptide acetyltransferase activity and POMC biosynthesis are coregulated.
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PMID:Coordinate regulation of peptide acetyltransferase activity and proopiomelanocortin gene expression in the intermediate lobe of the rat pituitary. 293 33

To investigate possible central dopaminergic regulation of beta-endorphin-like immunoreactivity (beta E-LI) and adrenocorticotropin (ACTH) release in humans, we gave the dopamine antagonist haloperidol or placebo intravenously to twelve normal male subjects and measured beta E-LI and cortisol for 120 minutes following injection. Haloperidol, but not placebo, produced significant increases in plasma beta E-LI and cortisol. These findings suggest that central dopaminergic pathways such as the tuberohypophyseal system may participate in regulation of the secretion of beta E and ACTH from the human pituitary.
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PMID:Haloperidol increases plasma beta endorphin-like immunoreactivity and cortisol in normal human males. 294 47

Intracerebroventricular administration of TRH induces excessive grooming behavior that is characterized by an important contribution of the elements scratching and paw licking. As compared with other grooming inducing peptides, the pattern of TRH-induced grooming resembles that induced by beta-endorphin rather than those elicited by ACTH or bombesin. TRH-induced excessive grooming is suppressed by pretreatment with haloperidol, naloxone or neurotensin. Haloperidol suppresses TRH-induced grooming in a general way, whereas the suppressive effect of the other drugs is mainly due to a selective reduction of TRH-induced excessive scratching. Combined treatments of rats with TRH and a submaximal dose of ACTH, bombesin or beta-endorphin do not result in higher grooming scores than with single peptide treatment. Excessive grooming elicited by water immersion is not affected by TRH. It is concluded that TRH is undoubtedly an excessive grooming inducing peptide. In situations where excessive grooming is elicited by other peptides or by water immersion, TRH does not further activate the operating systems involved in the existing excessive grooming.
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PMID:Some characteristics of TRH-induced grooming behavior in rats. 313 46


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