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

The effects on retrieval of a one-trial learning inhibitory avoidance response of beta-endorphin, alpha-endorphin, and gamma-endorphin, given prior to test have been studied in rats. beta-Endorphin (beta-LPH 61-91) in a relatively low dose (1.56 micrograms sc. or 50 ng icv.) facilitated inhibitory avoidance behavior, while a higher dose (10 micrograms sc. or 100 ng icv.) caused bimodal changes (facilitation in 50% of the animals and attenuation in another 40%. Peripheral injection of gamma-endorphin attenuated inhibitory avoidance behaviour in a dose-dependent manner. The C-terminus of beta-endorphin (beta-LPH 78-91) was ineffective. alpha-Endorphin facilitated inhibitory avoidance behavior in a dose dependent manner. Naltrexone pretreatment antagonized the bimodal effect of beta-endorphin: following pretreatment with the opiate antagonist the low latency component disappeared, but the facilitatory effect of the neuropeptide remained the same. It is suggested that beta-endorphin carries more than one bit of behavioral information. Inherent activities either related or unrelated to naltrexone-sensitive opiate as well as biotransformation into alpha- and gamma-endorphin may contribute to the multiple behavioral effects of this neuropeptide.
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PMID:Effects of beta-endorphin and its fragments on inhibitory avoidance behavior in rats. 620 40

The effects of the C-terminal octapeptide of cholecystokinin (CCK-8) and its related peptides on the onset and duration of beta-endorphin-induced catalepsy on injection of the peptides into the lateral ventricle were investigated in male rats. The onset of catalepsy was delayed to some extent by nonsulfated CCK-8 and CCK-7 but CCK-8 and caerulein were ineffective. Naltrexone and caerulein significantly shortened the duration of catalepsy, but CCKs were less effective to shorten it. Pentagastrin had no effect on either parameter.
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PMID:Suppressive effect of cholecystokinin and its related peptides on beta-endorphin-induced catalepsy in rats. 627 61

Naltrexone, an opiate antagonist, was administered to young obese (ob/ob) and lean mice for five weeks. Animals had continuous access to food and received 10 mg/kg SC twice daily with equivalent volumes of saline given to controls. The effects on body weight, and pituitary and plasma levels of beta-endorphin-like material were measured. Naltrexone-injected obese animals gained weight more slowly over the first three weeks while the weight gain of lean animals was not affected by naltrexone. Plasma levels of beta-endorphin were shown to be significantly higher in untreated ob/ob mice and this difference increased with age (4-20 weeks). With naltrexone treatment, plasma levels in +/? mice rose and exceeded those in ob/ob. Saline treatment appeared to be a stress, and pituitary beta-endorphins rose 4-6 fold in ob/ob compared with +/?. While naltrexone reduced the levels of ob/ob pituitary towards normal, no effect on beta-endorphin levels in pituitary of lean mice was obtained. In vitro studies of effects of the opiate antagonists, naloxone, on insulin secretion by isolated islets provided additional evidence of resistance of lean mice to naloxone relative to ob/ob. (IRI secretion fell only in naloxone treated ob/ob islets). These observations support the contention that this form of genetic obesity is characterized by elevated endogenous opiate levels and an increased sensitivity to opiate antagonists such as naltrexone or naloxone.
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PMID:Naltrexone reduces weight gain, alters "beta-endorphin", and reduces insulin output from pancreatic islets of genetically obese mice. 627 40

This study was designed to examine in rats the effects of systemic administration of a potent met-enkephalin analog, D-Ala2-met-enkephalinamide (DALA), on plasma ACTH and corticosterone secretion under basal conditions. Plasma radioimmunoassayable ACTH and corticosterone showed biphasic responses to intraarterial administration of DALA in chronically cannulated, conscious, freely moving, nonstressed animals. Both plasma ACTH and corticosterone increased at 5-10 min and decreased at 45-65 min after the administration of DALA (500 micrograms/kg) compared with either the basal concentrations or the corresponding responses in saline vehicle-injected control rats. Pretreatment with the specific opioid receptor antagonist naltrexone (2 mg/kg, intraarterially) completely prevented the DALA-induced increase in the plasma ACTH concentration and blunted the DALA-induced increase in the plasma corticosterone concentration. Naltrexone also increased plasma concentrations of ACTH and corticosterone above basal levels at a later time in DALA-treated animals. The DALA-induced increase in plasma corticosterone appears to be mediated by ACTH, mice DALA failed to increase plasma corticosterone in either hypophysectomized or dexamethasone-suppressed rats. DALA decreased the adrenocortical responsiveness to ACTH in hypophysectomized, but not in untreated or dexamethasone-suppressed, rats. Naltrexone increased the adrenocortical response to ACTH in DALA-treated rats. These data suggest that endogenous opioid peptides regulate pituitary-adrenocortical secretion under basal conditions by modifying both ACTH secretion and the glucocorticoid response to ACTH.
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PMID:D-Ala2-Met-enkephalinamide, a potent opioid peptide, alters pituitary-adrenocortical secretion in rats. 629 Jan 84

Opioid peptides have well-documented modulatory effects on the synaptic transmission of several neurotransmitters. In both hypothalamus and striatum there is dense innervation by the beta-endorphin and/or enkephalin neuronal systems, and physiologically relevant neuroregulatory interactions of these neurons occur with other important neurotransmitter neuronal systems, such as the dopaminergic tuberoinfundibular and nigroneostriatal systems. Previous reports have examined the effects of opioid peptides on release, synthesis and degradation of dopamine in these brain regions. In this report, we describe the effects of the intracerebral administration of beta-endorphin to increase dopamine (re)uptake by dopaminergic nerve terminals of the hypothalamus and striatum. The specific, high affinity uptake of [3H]dopamine by dopaminergic nerve terminals was studied in a synaptosomal preparation by pharmacological exclusion, using desmethylimipramine, of dopamine uptake into other monoaminergic nerve terminals. The augmentation of in vitro dopamine uptake in both hypothalamus and striatum following intracisternal administration of beta-endorphin is specifically mediated by opiate receptors, since it could be prevented by pretreatment with an opiate receptor antagonist, naltrexone. In hypothalamus, the increased dopamine uptake represents a primary effect of beta-endorphin on hypothalamic dopamine neurons and is not secondary to the opioid peptide-induced stimulation of prolactin secretion, since identical effects of beta-endorphin administration are seen in hypophysectomized and intact animals. The effect of beta-endorphin to increase hypothalamic dopamine uptake was not reflected by a change in the affinity constant for dopamine, but involved an increase in maximal initial velocity of uptake. Naltrexone blocked the effect of beta-endorphin to increase the Vmax for [3H]dopamine uptake by hypothalamic dopamine neurons in both intact and hypophysectomized rats. In vitro exposure of hypothalamic and striatal dopaminergic nerve terminals to a wide range of concentrations of beta-endorphin failed to reproduce the in vivo results; some concentrations of beta-endorphin produced small decreases in [3H]dopamine uptake which were not reversed by naloxone. The data of this study provide evidence for a further mechanism by which beta-endorphin may alter dopaminergic neurotransmission, namely by increasing dopamine reuptake into dopaminergic nerve endings.
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PMID:beta-Endorphin alters dopamine uptake by the dopamine neurons of the hypothalamus and striatum. 629 1

Two anorectic drugs which stimulate serotonin neuronal activity by releasing serotonin from nerve terminals, d-fenfluramine and CM 57 277 (4-amino-[6-chloro-2-pyridyl]-1-piperidine HCl), were studied in rats. Both drugs, when given for 5 days at doses of 15 mg of d-fenfluramine per kg/day and 20 mg of CM 57 277 per kg/day, decreased body weight gain and increased content of Met5-enkephalin and beta-endorphin in hypothalamus, but not in frontal cortex or pituitary. The increase in the hypothalamic content of the two opioid peptides elicited by d-fenfluramine was reversed by metergoline and p-chlorophenylalanine, suggesting that it is mediated by serotonin. The content of two other hypothalamic neuropeptides, cholecystokinin and substance P, were not affected by d-fenfluramine. Although Met5-enkephalin content in striatum was increased transiently by d-fenfluramine, this was not a serotonin-mediated effect because it was not abolished by metergoline. The decrease in body weight gain was prevented by metergoline, but not by i.p. injection of p-chlorophenylalanine. The effect of p-chlorophenylalanine on intestine may contribute to its failure in reversing the anorectic effect of d-fenfluramine. Naltrexone, an antagonist of opiate receptor, decreased body weight gain but exerted no effect on hypothalamic Met5-enkephalin or beta-endorphin content. Taking into consideration that the increase in Met5-enkephalin and beta-endorphin may have resulted from accumulation due to decreased utilization, the anorectic effects of serotonin releasing drugs may be mediated by a reduction in the functional role of hypothalamic opioid peptides.
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PMID:Accumulation of hypothalamic endorphins after repeated injections of anorectics which release serotonin. 629 96

The effects of the ACTH 4-9 analog (Org 2766) and the COOH-terminal tripeptide of Org 2766 (Phe-D-Lys-Phe; PDLP) on retrieval of one-trial learning passive avoidance behavior were compared with those of beta-endorphin, [Met5]-enkephalin, [D-Ala2,Met5]-enkephalin, des-Tyr1-[Met5]-enkephalin and des-enkephalin-gamma-endorphin (DE gamma E). Amounts of intracerebroventricularly administered Org 2766, PDLP, [Met5]-enkephalin, [D-Ala2,Met5]-enkephalin and DE gamma E, which induced a comparable attenuation of passive avoidance behavior were determined. Pretreatment with the opiate antagonist naltrexone prevented the attenuating effect of these peptides on passive avoidance behavior except that of DE gamma E. The attenuating effect of Org 2766 and of [Met5]-enkephalin was reversed to facilitation of passive avoidance behavior in the presence of naltrexone. Subcutaneous treatment with Org 2766 and [D-Phe7]-ACTH 4-10 decreased electrical self-stimulation behavior elicited from the medial septal area. Naltrexone prevented the inhibitory effect of Org 2766 on this behavior, but not that of [D-Phe7]-ACTH 4-10. Although the attenuating effect of PDLP on passive avoidance behavior was not reduced by pretreatment with [Met5]-enkephalin- or beta-endorphin-antiserum, and PDLP induced neither analgesia nor excessive grooming, the data suggest that the inhibitory effect of Org 2766 and PDLP on passive avoidance behavior and electrical self-stimulation are mediated by endorphin systems in the brain.
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PMID:Naltrexone-sensitive behavioral actions of the ACTH 4-9 analog (Org 2766). 630 25

The effects of chronic treatment with methadone, a long-acting opiate agonist, and naltrexone, a long-acting opiate antagonist on brain immunoreactive beta-endorphin (IR-beta-EP) concentrations were studied in the rat. Male rats were treated for 30 days with either methadone, 2.5 mg/kg/day; naltrexone 2 mg/kg/day, or saline. In a repeat experiment, rats were treated for 36 days with either methadone 2.5 mg/kg/day; naltrexone 4 mg/kg/day, or saline. Brain regions were homogenized in 0.2 N HCl and assayed for IR-beta-EP by RIA. No change in the IR-beta-EP content of the hypothalamus, thalamus, midbrain, or amygdala was measured in either experiment after methadone treatment. Naltrexone, however, significantly lowered brain IR-beta-EP in both experiments. In the first study hypothalamic IR-beta-EP fell from 189 +/- 17 (SEM) to 132 +/- 7.0 ng/g wet weight of tissue after naltrexone treatment (p less than 0.01). In the second experiment naltrexone lowered IR-beta-EP in the hypothalamus from 23.4 +/- 3.6 to 15.5 +/- 1.2 ng/mg protein (p less than 0.005). Similar decreases in the IR-beta-EP content of the thalamus (from 6.74 +/- 0.59 to 4.59 +/- 0.38 ng/mg protein) and amygdala (from 1.31 +/- 0.08 to 0.90 +/- 0.10) were also measured (p less than 0.01). We conclude that occupancy of opiate receptors by an opiate antagonist reduces brain levels of IR-beta-EP and suggests that chronic opiate receptor blockade may result in a compensatory increase in brain beta-EP release.
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PMID:Effect of chronic naltrexone and methadone administration on brain immunoreactive beta-endorphin in the rat. 631 67

A highly palatable diet (ordinary chow supplemented with 4 highly palatable items changes every day) (HPD) provokes hyperphagia and overweight in the rat. After 17 weeks of such a diet, naltrexone (0.5 or 2.5 mg/kg IP) and opiate antagonist, was injected at the beginning of the dark period, and a food intake test was performed during the 3 following hours. Naltrexone does not modify the energy intake in control rats receiving ordinary chow but suppresses HPD induced hyperphagia. The involvement of the beta-endorphin system in this type of hyperphagia is discussed.
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PMID:Naltrexone suppresses hyperphagia induced in the rat by a highly palatable diet. 729 Dec 35

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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