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 peptides corticotrophin releasing factor (CRF), ACTH4-10 and alpha-MSH have previously been shown to be behaviourally and neurochemically active. Using a passive avoidance task, we studied the effects of intra-ventricular administration of these peptides (0, 10 or 100 ng/rat) given either immediately following the learning trial, or 1 h prior to retention (24 h post-learning) test. We found that they affected behaviour; in some cases improving and in others disrupting performance. Statistical examination of the data suggests that these substances probably act on arousal mechanisms, in a manner reminiscent of the effects of vasopressin [13, 15].
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PMID:Corticotrophin releasing factor is more potent than some corticotrophin-related peptides in affecting passive avoidance behaviour in rats. 630 81

Rats were trained in a step-down inhibitory avoidance task using a small start platform (5-cm high, 25 X 7 cm) and a low intensity footshock (0.3 mA, 60 Hz). Retrieval of this task was measured on a test session 24 hr after training. The ip administration of ACTH1-24 (25 ng/rat), epinephrine HCl (625 ng/rat), or human beta-endorphin (125 ng/rat) 5 min prior to testing enhanced retrieval. beta-Endorphin was also effective when given by the icv route at a dose of 25 ng/rat. The icv administration of ACTH (5, 25, or 125 ng/rat) or epinephrine (5, 25, 125, or 625 ng/rat) was ineffective. These findings suggest that memory modulation by beta-endorphin at the time of retrieval may be centrally mediated, whereas the influence of ACTH and epinephrine is probably mediated peripherally.
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PMID:Effect of the intraperitoneal and intracerebroventricular administration of ACTH, epinephrine, or beta-endorphin on retrieval of an inhibitory avoidance task in rats. 632 57

The effect of the non-opiate beta-endorphin (beta E) fragment 2-9 and related peptides on immunoreactive (IR) arginine8 -vasopressin (AVP) levels was studied in the rat eye plexus plasma. Additionally, the effect of beta E 2-9 on AVP release from pituitary neurointermediate lobes ( NILs ), in vitro was studied. IR AVP levels in the eye plexus plasma increased after subcutaneous (s.c.) injection of beta E 2-9. In female rats peak values were observed 2 min after the administration of beta E 2-9 (10 micrograms/rat). Male rats were 100 times more sensitive than female rats. A dose-response study revealed a U-shaped relationship for this effect of beta E 2-9 in animals of both sexes. From structure-activity studies it appeared that beta E 2-9 was the most effective fragment. Intracerebroventricular (i.c.v.) administration of beta E 2-9 did not affect the IR-AVP levels in eye plexus plasma. Moreover, AVP release from the rat NILs cells in vitro was stimulated by perfusion with beta E 2-9, indicating a direct effect of the peptide on the pituitary. Therefore we suggest that beta E 2-9 increases AVP release by a direct action on the posterior pituitary.
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PMID:The stimulatory effect of a non-opiate beta-endorphin fragment on arginine-vasopressin release in rats. 633 Jun 64

The effect of subcutaneously injected DT gamma E (beta-endorphin, (beta E)2-17) on the pineal melatonin level was compared with that of closely related peptides and the neuroleptic drug haloperidol. As found previously, DT gamma E (3 ng/rat and 300 ng/rat) increased the melatonin levels. Similar doses of DT alpha E (beta E 2-16), DT beta E (beta E 2-31), gamma E (beta E 1-17), alpha E (beta E 1-16) and beta E failed to significantly change the melatonin levels in both the dark and the light phase. Haloperidol in a dose of 300 ng/rat exhibited a similar effect as DT gamma E.
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PMID:des-Tyr1-gamma-endorphin and haloperidol increase pineal gland melatonin levels in rats. 663 74

The protein kinase activities endogenous to synaptic membranes prepared by an identical procedure from avian (chick) and mammalian (rat) brains were compared. Both species showed similar responses towards both protein kinase effector molecules cyclic adenosine monophosphate and Ca2+. Kapp for cyclic adenosine monophosphate-dependent protein kinase activity occurred at 0.4-0.8 microM cAMP and Kapp for Ca2+-dependent, calmodulin-requiring protein kinase activity occurred at 1-2 microM Ca2+ (free ion concentration) both in the absence or presence of calmodulin added to the reaction mixture. This suggests that endogenous calmodulin in these membranes was able to modulate the Ca2+-dependent, calmodulin requiring protein kinase activity. After EGTA-treatment of the membranes to remove endogenous Ca2+ and calmodulin, no significant response towards Ca2+ on the phosphorylation of the membrane polypeptides was measured unless exogenous calmodulin was added after which the Kapp for Ca2+ was increased to 15 microM Ca2+ (free ion concentration). There was a difference in the maximal levels of kinase activity in these membranes with chick membranes containing 57% less cyclic adenosine monophosphate-dependent protein kinase activity, but 65% more Ca2+-dependent, calmodulin-requiring protein kinase activity than the rat membranes. Similar results were determined when either low (5 microM) or high (5.8 microM) concentrations of adenosine 5'-triphosphate were added to the reaction mixtures. Besides certain species differences in the molecular weights of the resulting phosphoproteins, we observed several major differences with respect to the absence or presence of some of the phosphoproteins. Chick synaptic membranes may lack the cyclic adenosine monophosphate-requiring, microtubule-associated phosphoprotein, MAP2, one of the 2 neurospecific, cyclic adenosine monophosphate-requiring and Ca2+, calmodulin-requiring phosphoproteins (Protein Ib, although Protein Ia apparently is present), and the Ca2+-requiring, calmodulin-independent, ACTH-sensitive phosphoprotein, B50. The phenothiazines, trifluoperazine, fluphenazine and chlorpromazine were found to inhibit the Ca2+-dependent, calmodulin-requiring protein kinase activities of both the chick and rat synaptic membranes. This inhibition appeared to be specific for calmodulin because at the same concentrations the phenothiazine analogue, chlorpromazine-sulfoxide, had no effect on this activity. Also found to inhibit Ca2+-dependent calmodulin-requiring protein kinase activity were dibucaine and adrenocorticotropin. These data suggest that rat forebrain synaptic plasma membranes are activated by cyclic adenosine monophosphate
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PMID:Endogenous protein phosphorylation in chick and rat brain synaptic membranes. 666 99

Pituitary opioid peptides levels, measured by guinea-pig ileum bioassay, have been evaluated in rats given single intracerebroventricular injections of alpha-methyl-p-tyrosine (4 mg/rat) or phentolamine (40 microgram/kg). Phentolamine produces an immediate rise in corticosteroid levels and an increase in pituitary endorphin content after 20 min. alpha-Methyl-p-tyrosine does not affect the pituitary endorphin levels, even if its effectiveness as a stressing agent is demonstrated by serum corticosterone increase and by reduced hypothalamic norepinephrine concentration. Repeated steroid treatment results in a decrease of serum corticosterone levels and of pituitary opioid activity. Such a decrease is mainly due to the reduction of beta-endorphin content, as shown by gel filtration analysis of pituitary extracts. It is suggested that the pituitary endorphin system, like ACTH, is under negative direct or indirect regulatory control of glucocorticoids. The adrenergic inhibitory tonus on pituitary opioid peptides, however, requires further confirmation.
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PMID:Role of adrenergic blocking agents and glucocorticoids on the regulation of pituitary opioid peptides levels. 722 9

In a previous study, we have shown that neuropeptide Y inhibits the release of alpha-melanocyte-stimulating hormone from the rat hypothalamus in vitro. The aim of the present study was to investigate the possible effect of neuropeptide Y on the regulation of proopiomelanocortin-derived peptides in vivo. Rats received acute or chronic administration of neuropeptide Y in the lateral ventricle and the amount of alpha-melanocyte-stimulating hormone was measured in the hypothalamus and in the neurointermediate lobe of the pituitary. In the same experiments, the amounts of corticotropin-releasing factor and corticotropin were quantified in the hypothalamus and anterior pituitary, respectively. Acute treatment with synthetic neuropeptide Y (0.1 to 10 micrograms/rat) did not modify the amount of alpha-melanocyte-stimulating hormone in the hypothalamus. In contrast, chronic infusion of neuropeptide Y (1.25 micrograms/h) over a seven day period significantly decreased the hypothalamic content of alpha-melanocyte-stimulating hormone, suggesting that neuropeptide Y regulates the synthesis and/or the processing of proopiomelanocortin. Concurrently, we found that both acute and chronic infusion of neuropeptide Y induced a significant reduction in corticotropin-releasing factor in the hypothalamus as well as a significant decrease in alpha-melanocyte-stimulating hormone and corticotropin in the neurointermediate and anterior lobes, respectively. Quantitative in situ hybridization histochemistry showed that chronic administration of neuropeptide Y also caused a reduction of proopiomelanocortin messenger RNA levels both in the intermediate and anterior lobes of the pituitary. Administration of neuropeptide Y (10(-6) M) on perifused rat hypothalamic slices caused a significant increase in corticotropin-releasing factor release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of centrally administered neuropeptide Y on hypothalamic and hypophyseal proopiomelanocortin-derived peptides in the rat. 747 27

Numerous studies have shown that interleukin 1 (IL1), a cytokine secreted by macrophages, is capable of stimulating the hypothalamo-pituitary-adrenal (HPA) axis. Nevertheless, the sites involved in IL1 stimulation of the HPA axis remain, to date, subjects of controversy. In the present study, using in vivo and in vitro approaches, we tried to characterize the route by which IL1 acts on the HPA axis. In vivo, after an i.p. injection of human IL1 beta (1 microgram/rat), we measured plasma ACTH concentration, anterior pituitary (AP) ACTH content, hypothalamic (HT) corticotropin releasing factor (CRF) content, and also AP pro-opiomelanocortin (POMC) and HT CRF gene expression. ACTH and CRF were measured by specific radioimmunoassays (RIAs), and solution hybridization nuclease protection assay was used for quantification of nuclear POMC precursor RNA and nuclear and cytoplasmic POMC and CRF mRNA. Human IL1 beta provoked an increase in ACTH plasma concentration, a decrease in AP ACTH content, and a prolonged increase in AP POMC primary transcript levels (around 100%). A significant increase in AP POMC primary transcript content was evident 30 min after injection of hIL1 beta, while cytoplasmic POMC mRNA levels were increased in the AP only at 4 hr after injection of hIL1 beta. We did not observe an effect of hIL1 beta on either HT CRF content or HT CRF cytoplasmic mRNA levels. In order to characterize a possible direct effect of hIL1 beta at the AP level, we used an AP perifusion system to analyse the effect of hIL1 beta and CRH on ACTH release and on POMC gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human interleukin 1 beta: corticotropin releasing factor and ACTH release and gene expression in the male rat: in vivo and in vitro studies. 751 72

The role of brain-gut peptide galanin in the regulation of prolactin (PRL) and beta-endorphin (beta-EP) release from anterior pituitary lobe was studied in vivo in conscious male rats and in vitro with cultured anterior pituitary cells of the rat. Galanin (1 microgram or 3 micrograms/rat) injected into the third cerebral ventricle of rats produced highly significant, dose-related increases of PRL resting secretion, but did not alter resting secretion of beta-EP and restraint stress-induced release of PRL and beta-EP. However, galanin (0.05, 0.5 and 1.0 micrograms/5 x 10(5) cells.ml-1) induced highly significant, dose-related increase of beta-EP secretion from dispersed anterior pituitary cells, but failed to alter significantly PRL secretion from the cultured cells. These results indicate that central galanin has a stimulatory role in pituitary PRL resting secretion via the hypothalamus, whereas peripheral galanin stimulates beta-EP secretion only via direct action of this peptide in anterior pituitary cells.
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PMID:[Regulatory role of galanin on prolactin and beta-endorphin release from anterior pituitary lobe of rat]. 754 Mar 17

In 28 month-old male rats, the i.c.v. injection of adrenocorticotropin [ACTH-(1-24)] (4 micrograms/rat) did not induce the typical behavioral syndrome (excessive grooming, stretching, yawning, penile erections). This indicates that the behavioral effects of melanocortins are age-dependent, suggesting either an aging-linked impairment of the nervous circuitries involved or a reduction of the number (or affinity, or both) of the brain melanocortin receptors in the elderly.
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PMID:Old rats are unresponsive to the behavioral effects of adrenocorticotropin. 770 25


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