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 release of melanophore stimulating hormone (MSH) from the pars intermedia of the amphibian Xenopus laevis is regulated by multiple factors of hypothalamic origin. The aim of this study was to determine if potential secretagogues function through a direct action on the melanotrope cell. For this purpose an in vitro superfusion system containing isolated melanotropes (cell suspension) was utilized. The viability of the cells in suspension was tested by examining their ability to synthesize, process and release pro-opiomelanocortin (POMC) related peptides. All biosynthetic functions appeared normal, with the exception that the isolated melanotropes are unable to N-terminally acetylate MSH. Release of immunoreactive-MSH from these cells was shown to be Ca2+-dependent, and high K+ stimulated release. Both the neurotransmitters dopamine and gamma-aminobutyric acid (GABA), which are thought to be physiologically important MSH-release inhibiting factors, were shown to inhibit MSH release from isolated melanotropes. Dopamine appeared to function through a dopamine D2 type receptor mechanism while for GABA, both a GABAa and GABAb receptor mechanism are involved.
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PMID:GABA and dopamine act directly on melanotropes of Xenopus to inhibit MSH secretion. 380 32

Dopamine is likely an important physiological melanotropin release-inhibiting factor in amphibians. This study concerns the effects of dopamine on the biosynthesis and release of peptides from the pars intermedia of the frog Rana ridibunda. Our results show that this secretagogue has no immediate effects on either the rate of biosynthesis of pro-opiomelanocortin nor on the direction of processing of this prohormone. Pulse-chase experiments revealed that dopamine inhibited the release of all newly synthesized POMC-related peptides in a dose-dependent manner. For each dopamine concentration tested, the degree of inhibition exerted on the release of the various newly synthesized peptides by a given concentration of secretagogue was approximately the same, with the exception of that found for the alpha-MSH related peptides. Analysis of the release of these melanotropins was complex because dopamine not only inhibited their release but also, either directly or indirectly, inhibited the acetylation reaction which converts des-N alpha-acetyl alpha-MSH to alpha-MSH. Dopamine was shown to be less potent in inhibiting the release of des-N alpha-acetyl alpha-MSH than inhibiting release of the acetylated form of the peptide. In amphibians a preferential release of the less-bioactive non-acetylated form of MSH under inhibitory conditions induced by dopamine may be of physiological importance.
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PMID:Regulation of biosynthesis and release of pars intermedia peptides in Rana ridibunda: dopamine affects both acetylation and release of alpha-MSH. 408 Jun 8

[3H]-Dopamine was found to be released from the rabbit retina in vitro by light stimulation, by 40 mM K+, and by alpha-MSH (alpha-Melanocyte-Stimulating Hormone) down to about 10(-7) M. The effect of alpha-MSH was dose-dependent. A number of known and putative retinal neurotransmitters and agonists (GABA, muscimol, glutamic acid, kainic acid, glycine, and carbachol, all 10(-4) M) were without significant effect. The results show that it is unlikely that there are excitatory receptors on the retinal dopaminergic neurons to any of the conventional transmitters. Further, alpha-MSH seems of interest as a possible neuroactive retinal substance, which was previously not been suspected.
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PMID:[3H]-dopamine release from the rabbit retina. 611 Dec 60

(1) The gonadotropins are secreted in a pulsatile fashion in response to the similar pulsatile release of GnRH from neurosecretory neurons centered in the arcuate nucleus of the medial basal hypothalamus. (2) The gonadal steroids appear to exert their feedback effects both directly on the pituitary and through modulation of the pulsatile pattern of GnRH secretion. They may also influence the degree of sialylation and subsequent biologic activity of the gonadotropins. (3) GnRH release is under the control of catecholaminergic neurotransmitters. Norepinephrine appears to act as an excitatory agent, whereas dopamine inhibits GnRH secretion. (4) Dopamine also directly inhibits PRL release and may be the prolactin-inhibiting factor. (5) The endorphins are endogeneous opiate peptides and are derived from a common ACTH/ beta-lipotropin precursor. Through modulation of neurotransmitter mechanisms, the endorphins may affect both PRL and gonadotropin secretion. (6) The catecholestrogens, by virtue of their structural similarity to the neurotransmitters, may mediate the central feedback actions of the gonadal steroids.
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PMID:The endocrinology of the menstrual cycle: the interaction of folliculogenesis and neuroendocrine mechanisms. 612 37

The perfused, isolated, pituitary cell column was used to measure the release of alpha-melanotropin (alpha-MSH)-like immunoreactivity (LI), carboxyl terminal corticotropin (C-ACTH)-LI, gamma-lipotropin (gamma-LPH)-LI, alpha-endorphin-LI, beta-endorphin-LI and amino-terminal pro-opiocortin (N-POC)-LI from rat pars intermedia (PI) cells. Concomitant secretion of all PI peptides was observed during basal release and in response to all applied stimuli. Dopamine (DA) caused a dose-dependent (10(-9)-10(-5) M) simultaneous inhibition of peptide release which was antagonised by haloperidol. Isoprenaline stimulated the release of PI peptides in a parallel, dose-related (10(-10)-10(-6) M) manner and was blocked by propranolol. Stimulation of peptide secretion caused by low concentrations (10(-8) M), of adrenaline (AD) and noradrenaline (NA) changed to inhibition at high concentrations (10(-5) M) whereas intermediate concentrations (10(-6), 10(-7) M) possessed both inhibitory and excitatory effects. A 45 mM solution of K+ ions stimulated the release of PI peptides and both the K+-stimulated secretion and basal secretion were Ca++-dependent. MSH-release-inhibiting factor (MIF) and 5-hydroxytryptamine (5-HT) failed to alter peptide secretion from the perfused PI cells. We conclude that pro-opiocortin (POC) peptides are released concomitantly from rat PI cells and that biogenic amines are involved in their release.
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PMID:Secretion of pro-opiocortin peptides from isolated perfused rat pars intermedia cells. 613 22

Extracellular recordings of 191 neostriatum neurons revealed the effects of ionophoretically applied dopamine, met-enkephalin and morphine on spontaneous and glutamate- and acetylcholine-evoked unit activity. Dopamine either depressed or enhanced the spontaneous and glutamate-evoked activities depending on the firing rate. Met-enkephalin depressed the spontaneous, glutamate- and acetylcholine evoked activities. These findings suggest that dopamine exerts a modulatory effect on glutamatergic synaptic neurotransmission in the rat neostriatum.
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PMID:[Effect of dopamine and met-enkephalin on the background and evoked spike activity of rat neostriatal neurons]. 615 23

Dopamine causes a dose-dependent contraction of the rat rectum in vitro followed by a relaxation. This contraction can be inhibited by apomorphine and phenylephrine. This inhibition can be attenuated by the beta-endorphin (beta E) fragments 2-17 (des-Tyr1-gamma-endorphin, DT gamma E) and 6-17 (des-enkephalin-gamma-endorphin, DE gamma E). beta E 6-17 seems to be the shortest sequence with full activity in this respect since a shorter fragment (beta E 10-17) was less effective. The atypical neuroleptics oxypertine, sulpiride, and clozapine, the classic neuroleptic haloperidol and metoclopramide have a similar action to DE gamma E. The peptides and atypical neuroleptics do not affect the dopamine response per se while the classic neuroleptics haloperidol and metoclopramide enhance the dopamine response. The effects of the alpha-type endorphins are opposite to those of the gamma-type endorphins, since des-Tyr1-alpha-endorphin (DT alpha E, beta E 2-16) and des-enkephalin-alpha-endorphin (DE alpha E, beta E 6-16) enhance the phenylephrine-induced decreased responsiveness to dopamine. Structure-activity studies revealed that the active moiety of the alpha-endorphin fragments probably resides in the 6-9 region. In addition the alpha-type endorphins directly inhibit the dopamine response. It is concluded that the rat rectum may be used to analyse neuroleptic-like action. In this model alpha- and gamma-endorphin fragments may directly or indirectly influence the interaction of dopamine with the rectum. Because of the strong similarities between the effects of gamma-type endorphins and that of neuroleptics the results support the purported neuroleptic-like action of gamma-type endorphins. The influence of alpha-type endorphins and gamma-type endorphins on the apomorphine or phenylephrine induced decreased responsiveness to dopamine, although opposite, seems to be mediated by an influence on different dopamine sensitive systems.
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PMID:Opposite interactions between alpha- and beta-endorphin fragments with dopamine mediated responses on the rat rectum in vitro. 618 56

Adult male Fischer-344 rats were dosed sc with 1 or 2.5 mg/kg of triethyl lead chloride (TEL) for 5 consecutive days. One week after the last dose, TEL-exposed rats had decreased Met-enkephalin in the hypothalamus, septum, and frontal cortex, while substance P was decreased in the hippocampus and frontal cortex. Dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in the caudate nucleus were not altered by TEL nor were serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the caudate nucleus, hypothalamus, hippocampus, or frontal cortex. In a second experiment, rats were dosed with 1.75 mg/kg sc for 5 days. Subsequent assay of brain tissue indicated that TEL decreased met-enkephalin levels in the septum of rats one and seven days after cessation of dosing; effects on substance P were not observed. TEL-induced decreases in Met-enkephalin in the septum were temporally associated with increased hot plate latencies. One day after cessation of dosing with TEL, concentration of 5-HIAA in the caudate nucleus, hippocampus, frontal cortex, and brain stem, and 5-HT in the hippocampus and brain stem were increased. Biogenic amine concentrations were not affected in any other region or at any other time postdosing. A third experiment indicated that TEL-induced analgesia could be attenuated by 10 mg/kg chlordiazepoxide or 10 mg/kg of naloxone. The present results suggest that TEL-induced analgesia may be due to alterations in emotionality or reactivity to noxious stimuli, which may be associated with the alteration in delta opiate mechanism in the limbic system, such as the change of septal enkephalin neuronal activities.
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PMID:Correlation of neurochemical and behavioral effects of triethyl lead chloride in rats. 619 48

The immunologic patterns of 3 human pituitary adenomas of Cushing's disease have been studied after gel exclusion chromatography (Sephadex G-50). The immunologic characteristics were examined with three radioimmunoassays specific for human corticotropin (ACTH), lipotropin (LPH) and beta-endorphin (beta-End). In cell tumor extracts, chromatographic peaks corresponding to beta-LPH, gamma-LPH, beta-End and ACTH were identified. The ACTH/beta-LP-beta-End ratio was 1 in the 3 cases. Additionally, in the 3 cases, a chromatographic peak, partially cross-reacting in the beta-End assay, was eluted after beta-End, thus suggesting the presence of a fragment of the molecule. In 1 case, a peak of large molecular weight material with N- and C-terminal beta-LPH and ACTH immunoreactivity was observed, which corresponded to the precursor material. The release and the effects of various stimuli were studied on dispersed tumor cells in primary culture. The tumor cells had a biphasic basal secretion rate with a rapid increase of ACTH/beta-LPH-beta-End in the culture medium during the first 2 h. Then the release, studied during 2 days, was slower. Chromatographic studies showed that the beta-LPH/beta-End ratio was 0.8 in the cells and 0.3 in the medium, due essentially to the release of beta-End and beta-End-like materials. The cells released ACTH and beta-LPH-beta-End in equimolar ratio after stimulation with arginine vasopressin (AVP). The maximum effect was obtained with 10(-6) M AVP (D50 = 1 10(-9) M). Dibutyryl cyclic AMP (2. 10(-3) M) induced maximal release of ACTH/beta-LPH-beta-End. This stimulation was suppressed by a 48-hour preincubation with dexamethasone (10(-8)-10(-6) M). There was no effect of TRH and LH-RH on cell release. Dopamine (10(-6) M) specifically blocked the release of ACTH/beta-LPH-beta-End in 1 case. These data showed (a) heterogeneity of chromatographic profiles from case to case; (b) the presence of material in the tumor, cell extracts and culture medium corresponding to fragment(s) of beta-End; (c) culture studies demonstrated that tumor cells remain responsive to AVP stimulation and dexamethasone suppression, and (d) the dopamine inhibition of ACTH and beta-End release needs further investigation.
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PMID:[Lipocorticotropic peptides in Cushing's disease: in vitro studies]. 626 12

Dopamine regulates the secretion of pituitary hormones: it inhibits permanently the production of prolactin and blocks the gonadotrophins and the thyroid-stimulating hormone. It stimulates inconstantly the secretion of growth hormone and it does not control corticotropin. Dopamine agonists and antagonists are currently used in the investigation and the treatment of hyper-prolactinemia and acromegaly.
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PMID:[Dopamine and pituitary hormones. Physiology and pathology (author's transl)]. 628 97


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