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)

Chronic administration of haloperidol (1 mg/Kg) into rats led to a marked increase in the level of beta-endorphin related peptides in the pars intermedia and brain stem. Using a combination of ion-exchange chromatography and radioimmunoassay, the increase in beta-endorphin under haloperidol treatment was confined to the acetylated derivatives: alpha,N-acetyl beta-endorphin 1-26, alpha,N-acetyl beta-endorphin 1-27 and alpha,N-acetyl beta-endorphin 1-31; there was no change in the level of the NH2-peptides. Haloperidol had no effect on the beta-endorphin related peptides in the anterior pituitary or hypothalamus. These findings suggest that haloperidol can influence not only the level of beta-endorphin related peptides in pituitary and brain, but also their posttranslational processing, possibly serving to regulate the level of biologically active beta-endorphin 1-31.
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PMID:Beta-endorphin processing in pituitary and brain is sensitive to haloperidol stimulation. 315 37

The intracerebroventricular (i.c.v.) injection of oxytocin, in doses ranging from 5 to 90 ng (5-90 pmol) induced penile erection and yawning in male rats. Such response was not induced by doses of the peptide higher than 100 ng, nor by equimolar doses of i.c.v. [Arg8]vasopressin, ACTH-(1-24), alpha-MSH, rat corticotropin-releasing factor (rCRF), delta sleep-inducing peptide, neurotensin or substance P. Oxytocin-induced penile erection and yawning were prevented by atropine and morphine, but not by methylatropine or the opiate antagonist naloxone. Haloperidol, a dopamine receptor antagonist, was ineffective at low doses; it partially prevented penile erection but not yawning at high doses. Since oxytocin is present not only in the neurohypophysis but also in other brain areas, our results suggest that oxytocin is implicated in the regulation of penile erection and yawning, and provide further evidence that oxytocin acts as a neuropeptide in the central nervous system.
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PMID:Oxytocin: an extremely potent inducer of penile erection and yawning in male rats. 379 49

We have compared immunoreactive beta-endorphin (ir-beta EP) levels in plasma, hypothalamus, anterior pituitary and neurointermediate lobe of adult female Sprague-Dawley rats, in studies in which levels of catecholamines were manipulated. Whole-brain catecholamines were manipulated by intraperitoneal haloperidol and/or bromocriptine; median eminence and neurointermediate lobe catecholamines were manipulated specifically and differentially by intravenous 6-hydroxydopamine (6-OHDA), with and without pretreatment with intraperitoneal desipramine; changes in amine neurons were assessed by fluorescence histochemistry. Haloperidol and 6-OHDA administration produced a selective reduction of neurointermediate lobe ir-beta EP, to levels equivalent to those seen with prolonged stress; the haloperidol effect was blocked by bromocriptine and the 6-OHDA effect by desipramine. Specific depletion of catecholamine nerve terminals in the median eminence and the neurointermediate lobe was associated with elevated plasma ir-beta EP, with no changes in pituitary or hypothalamic levels. These studies confirm and extend previous reports documenting that ir-beta EP levels in different tissues are modulated by different neural stimuli.
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PMID:Stress, dopaminergic blockade and median eminence-neurointermediate lobe catecholamine depletion: effects on hypothalamic, pituitary and plasma immunoreactive beta-endorphin. 608 92

Methergoline, an antagonist of cerebral serotonin receptors, has been shown to significantly reduce the rise in rectal temperature (Tre) produced by the intracerebral microinjection of beta-endorphin. In this study the role of serotonin in the increase in Tre elicited by beta-endorphin was further examined using three additional serotonin antagonists. beta-Endorphin was administered twice to rats using a crossover design in which half of the animals were first pretreated with the vehicle solution and half with the antagonist. Serotonin antagonists used were: methergoline, methysergide, cinanserin and cyproheptadine. Although methergoline did cause a marked reduction in the beta-endorphin-induced rise in Tre, neither methysergide, nor cinanserin, nor cyproheptadine produced a marked reduction in the hyperthermia. Since methergoline also interacts with the dopamine receptor, the effect of a dopamine antagonist, haloperidol, on the endorphin-evoked response was also examined. Haloperidol failed to attenuate the rise in Tre. The reason for the apparent discrepancy in the action of these serotonin antagonists is unclear. Further research may reveal distinct subpopulations of serotonin receptors at which these antagonists exert differential effects.
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PMID:Action of selected serotonin antagonists on hyperthermia evoked by intracerebrally injected beta-endorphin. 627 Jun 36

Haloperidol (0.03-3 mg/kg) dose-dependently increased the plasma concentrations of immunoreactive beta-endorphin (ir-beta-END) without changing the concentrations of ir-beta-END in the adenohypophysis or the neurointermediate pituitary of rats. Elevated levels of ir-beta-END in plasma were also found after chronic treatment with haloperidol (1 mg/kg per day) for 3 weeks. The long-term treatment, however, caused a selective increase (60%) of the ir-beta-END concentrations in the neurointermediate pituitary without changing that in the adenohypophysis. Significantly elevated levels of ir-beta-END were also found in the hypothalamus and the septum. Gelchromatographic separation of the plasma components reacting with the beta-endorphin antiserum revealed that both the acute and chronic haloperidol treatment increased the plasma concentrations of immunoreactive material with the molecular size of beta-endorphin and beta-lipotropin. This indicates that, at least, part of ir-beta-END released by haloperidol into plasma is of adenohypophyseal origin, since no material with the molecular size of beta-lipotropin has been found in the neurointermediate pituitary.
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PMID:Effects of acute and chronic haloperidol treatment on the concentrations of immunoreactive beta-endorphin in plasma, pituitary and brain of rats. 627 59

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 influence of systemically administered Des-Tyr1-alpha-endorphin (DT alpha E), Des-Tyr1-gamma-endorphin (DT gamma E) and haloperidol on electroencephalographic (EEG) activity of the lateral septum complex (LSC) and the frontal cortex was studied in male rats. DT alpha E (2 micrograms) significantly increased whereas DT gamma E (10 micrograms) significantly decreased the amounts of activity in the 5 Hz band. In addition, DT alpha E promoted production of 15-20 Hz activity, while DT gamma E decreased the amount of 20-30 Hz activity. EEG activity exhibited a marked variability which persisted throughout the recording session following administration of the peptides. Haloperidol markedly decreased the proportion of 10-15 Hz activity. The alterations in EEG of the frontal cortex were similar to those in LSC but less pronounced. The differences in the time course and frequency bands affected suggest that the effects of peptides and haloperidol on EEG activity of LSC are not mediated by the same mechanisms.
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PMID:Electroencephalographic changes in the lateral septum complex following systemic administration of des-Tyr1 -alpha-endorphin, des-Tyr1-gamma-endorphin and haloperidol in rats. 715 42

A single dose of 0.5 micrograms beta-endorphin injected intraventricularly in unanesthetized male rats bearing chronic intraventricular and intrajugular cannulas led to a sevenfold stimulation of plasma prolactin (PRL) levels 10 to 20 min after injection of the peptide, while a dose of 2 micrograms of beta-endorphin led to a comparable stimulation of plasma growth hormone (GH) concentration. Met-Enkephalin was much less potent than beta-endorphin in stimulating PRL and GH release. Naloxone, a specific opiate antagonist, completely blocked the stimulation of GH and PRL release at the doses of 0.5 and 12.5 mg/kg, respectively. beta-Endorphin and Met-enkephalin from 41 discrete brain nuclei were measured by radioimmunoassay (RIA). beta-Endorphin was found in the hypothalamus medial preoptic nucleus, nucleus interstitialis striae terminalis (NIST), nucleus medialis thalami, and periaqueductal gray. Met-Enkephalin was found predominantly in the globus pallidus, NIST, medial preoptic nucleus, nucleus amygdaloideus centralis, and nucleus lateralis hypothalami. Treatment with both estrogens and haloperidol led to differential effects on Met-enkephalin content in various brain nuclei. Estrogen treatment increased Met-enkephalin levels in globus pallidus, NIST, medial and lateral preoptic nuclei, and periaqueductal gray, while a decrease of the Met-enkephalin content in the nucleus amygdaloideus centralis was found. Haloperidol treatment led to a stimulatory effect in striatum, medial and lateral preoptic nuclei, and interpeduncular nucleus.
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PMID:beta-Endorphin and met-enkephalins: their distribution, modulation by estrogens and haloperidol, and role in neuroendocrine control. 738 27

We examined the effect of chronic administration (14 days) of haloperidol (2 mg/kg/day) or sulpiride (100 mg/kg/day), on the mRNA levels of various genes in the rat striatum and pituitary by quantitative in situ and Northern blot hybridizations. In the pituitary, haloperidol and sulpiride induced similar increases of mRNAs of pro-opiomelanocortin (POMC) (+65% and +73%), prolactin (PRL) (+821% and +840%) and growth hormone (GH) (+32% and +47%), but sulpiride induced a greater increase of D2R mRNA (+125%) than haloperidol (+92%). In the striatum, sulpiride and haloperidol had different effects: sulpiride induced a higher increase than haloperidol of both preproenkephalin A (PPA) mRNA (+67% versus +47%) and D2 dopamine receptor (D2R) mRNAs (+72% versus +40%). Moreover, haloperidol and sulpiride had opposite effects on substance P (SP) mRNA. Haloperidol decreased the amount of SP mRNA by 20% while sulpiride increased it by 20%. The D1 dopamine receptor (D1R) mRNA level was not significantly modified after either treatment. Our results demonstrate that the effect of a chronic haloperidol treatment on striatal dopamine receptors and neuropeptide mRNA levels is different to that of sulpiride, whereas it is similar on pituitary hormones mRNA levels.
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PMID:Differential influence of haloperidol and sulpiride on dopamine receptors and peptide mRNA levels in the rat striatum and pituitary. 751 29

The exposure of rat brain slices containing caudate putamen and accumbens nuclei to alpha-MSH or dopamine (DA) results in an increase in cyclic AMP (cAMP) levels. When tissues are compared with those containing both alpha-MSH and DA, a reduction in the cyclic nucleotide is observable. This study was carried out to determine whether variations in tissular cAMP levels induced by alpha-MSH might be explained by an interaction between the peptide and some dopaminergic receptors. Therefore, we measured cAMP in tissues and medium in response to alpha-MSH in the presence of haloperidol, the selective D1 (SCH 23390) or D2 (sulpiride) antagonists, or the selective D1 (SKF 38393) or D2 (bromocriptine) agonists. Haloperidol by itself induced no changes either in the cAMP content or in the cAMP efflux to the medium. When slices were exposed to alpha-MSH and haloperidol, the latter blocked the alpha-MSH effect of inducing an increase in the content of cAMP. None of the specific antagonists (at the administered doses) induced changes in the content of cAMP when compared with the control group. The presence of SCH 23390 in the incubation medium together with alpha-MSH yielded a reduction in cAMP levels compared with those incubated with alpha-MSH. A slight stimulatory effect on cAMP formation was observed when the dopaminergic agonists (SKF 38393 10 microM) were used. We conclude that alpha-MSH interacts with the D1 dopamine receptor, changing the cAMP levels in striatum and accumbens nuclei.
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PMID:alpha-MSH changes cyclic AMP levels in rat brain slices by an interaction with the D1 dopamine receptor. 771 65


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