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)

Acute ethanol exposure produces activation of the brain-pituitary-adrenal (BPA) axis, resulting in the release of ACTH, beta-endorphin, and glucocorticoids. While elevated levels of plasma glucocorticoids are also found after chronic ethanol administration, plasma ACTH and beta-endorphin are normal or reduced. It is also unclear whether chronic ethanol exposure results in tolerance to the stimulatory effect of ethanol on BPA activity. To determine the site and mechanism of ethanol action on the BPA axis we studied the CRF secretory profile in a superfused rat hypothalamic preparation after chronic ethanol administration in vivo and the CRF responses after acute ethanol exposure in vitro. Superfused hypothalami from normal and pair-fed control rats released CRF-like immunoreactive material (CRF-LI) in a pulsatile manner, with a mean (+/- SE) frequency of 5.1 +/- 0.7 pulses/h. In contrast, the pulse frequency of CRF-LI release from hypothalami of rats receiving chronic ethanol treatment (fed an alcohol-containing liquid diet for 2 weeks) increased dramatically; the basal mean CRF level, pulse amplitude, and pulse duration remained unchanged. Hypothalamic CRF content was decreased. This chronic ethanol exposure also altered the dose-response characteristics of CRF release when ethanol was introduced acutely, as a pulse, into the in vitro preparation. Acute exposure to 20 mg/100 ml ethanol produced greater release of CRF-LI from control hypothalami than from chronic ethanol-exposed hypothalami. A further elevation above basal levels was produced by 200 mg/100 ml ethanol in control, but not ethanol-exposed, hypothalami. Secretion of CRF from ethanol-exposed hypothalami in response to depolarizing concentrations of potassium chloride was suppressed. Chronic ethanol treatment had no effect on CRF-LI and CRF bioactivity responses to stimulation with acetylcholine. These findings suggest the presence of a high frequency pulse-generating mechanism for CRF release in the hypothalamus. This pulsatile secretory mechanism is altered by chronic ethanol exposure of the animals in vivo. Chronic intoxication resulted in tolerance to the stimulatory effect of ethanol on CRF release in vitro.
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PMID:Effects of ethanol on CRF release in vitro. 284 85

The ionic conductance mechanisms underlying the action potential behaviour of frog melanotrophs in primary culture were studied by using the patch-clamp technique in whole-cell configuration. The action potentials spontaneously generated by these cells were predominantly sodium spikes with a calcium component. Voltage-dependent sodium, calcium, potassium and calcium-activated potassium currents were identified and analysed separately. The voltage-dependent sodium current was characterized by its fast kinetic, its low-threshold activation, its voltage-dependent inactivation and a tetrodotoxin sensitivity. Calcium currents were identified on the basis of their ionic selectivity to divalent cations (Ba2+, Ca2+, Co2+) and their time course. Only two of the three well-documented calcium currents could be detected in frog melanotrophs. A sustained calcium current (ICaS) and an inactivating calcium current (ICaN) were elicited by step depolarizations up to -20 mV. ICaN inactivated for membrane potentials more positive than -50 mV; its inactivation appeared to be both voltage- and calcium-dependent. Transient calcium current (ICaT) has never been observed. Two types of potassium currents were identified: voltage-dependent potassium (IKV) and calcium-activated potassium currents, (IK[Ca]). They were both suppressed by tetraethylammonium chloride, whereas only IK(Ca) was blocked by cobalt. These major ionic currents underlying spontaneous electrical activity are assumed to be involved in the process of alpha-melanocyte-stimulating hormone release. The present study provides the ground for future investigations regarding the relationships between the electrical and secretory activities in amphibian pars intermedia cells.
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PMID:Patch-clamp study of the ionic currents underlying action potentials in cultured frog pituitary melanotrophs. 285 22

Acute changes associated with removal of the inhibition of estrus caused by suckling were examined in beef cows. Calves were weaned during the fifth week after parturition and cows were slaughtered at 0 (n = 8), 36 (n = 8) or 72 h (n = 8) after calf removal. Tissues of preoptic area (POA), hypothalamus (HYP), pituitary stalk-median eminence (SME) and pituitary neurointermediate lobe (NIL) were obtained for analyses of luteinizing hormone-releasing hormone (LHRH) and four opioid neuropeptides. In addition, one-half of each SME was superfused in vitro for measurement of basal and potassium-induced release of LHRH. The following opioid neuropeptides were quantified: methionine-enkephalin (Met-Enk), beta-endorphin (beta-EP), dynorphin-A, 1-17 (DYN-17) and dynorphin-A, 1-8 (DYN-8). All four opioid neuropeptides were most concentrated in the pituitary NIL. Luteinizing hormone-releasing hormone was most concentrated in the SME tissue, which also contained substantial concentrations of Met-Enk and beta-EP, but very little DYN-17 or DYN-8. In addition, weaning increased the weight of NIL between 0 and 36 h (P less than .05), and the concentrations of LHRH, Met-Enk, and DYN-17 in the combined POA + HYP (P less than .05) tissue between 36 and 72 h. No differences occurred among groups in SME content of LHRH or in vitro release of LHRH from the superfused SME. Although they were not affected by weaning, within-cow correlations among parameters revealed that: 1) concentrations of DYN-17 and DYN-8 were always positively correlated (P less than .05); 2) concentrations of LHRH were positively correlated with Met-Enk (P less than .01), beta-EP (P less than .05) and DYN-17 (P less than .05) in the combined POA + HYP tissue; 3) LHRH concentrations in SME tissue were negatively related to POA + HYP concentrations of Met-Enk (P less than .01) and beta-EP (P less than .05), but not of LHRH or DYN-17 and 4) in vitro release of LHRH from the pituitary SME was correlated with concentrations of DYN-8 in various tissues including the SME (P less than .01). In summary, bovine neural tissues differ widely in concentrations of the four opioid neuropeptides with NIL tissue having the greatest concentrations. Weaning calves at 36 and 72 h before slaughter caused parallel changes in LHRH, Met-Enk and DYN-17 in preoptic and hypothalamic tissues.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relationships among concentrations of four opioid neuropeptides and luteinizing hormone-releasing hormone in neural tissues of beef cows following early weaning. 287 Oct 5

LHRH has previously been found to be the only known hypothalamic releasing factor which can specifically stimulate the release of the opioid dynorphin and other proenkephalin B-derived peptides from the rat adenohypophysis in vitro. In the present study the mechanisms that regulate dynorphin release were further characterized. It was examined whether or not dynorphin release from the adenohypophysis in vitro is altered during inhibition of the secretion of various anterior pituitary hormones. Rat anterior pituitary quarters were incubated in vitro and hormone release into the incubation medium was measured by RIAs. Somatostatin, dopamine, T3, dexamethasone, and 5 alpha-dihydrotestosterone were used to inhibit the secretion of GH, PRL, TSH, ACTH/beta-endorphin, or LH/FSH, respectively. GH, PRL, or beta-endorphin release was inhibited without affecting the simultaneous release of dynorphin A-(1-13)-like immunoreactivity (Dyn A1-13-IR). Concentrations of T3, somatostatin, or dopamine which were effective in suppressing the evoked and/or basal release of TSH, GH, or PRL, respectively, produced no effect on Dyn A1-13-IR release caused by high potassium concentration (40 mM) or LHRH (500 pM). The LHRH-induced release of LH and FSH was inhibited by the glucocorticoid dexamethasone or the androgen 5 alpha-dihydrotestosterone. Under these conditions, Dyn A1-13-IR release was also reduced. However, whereas LH release was completely blocked by 5 alpha-dihydrotestosterone, FSH and Dyn A1-13-IR release was reduced only by 50%. The release of FSH and Dyn A1-13-IR in vitro from anterior pituitary glands taken from rats, castrated 3 weeks before, was enhanced to a similar extent (about 2.5-fold); the simultaneous enhancement of LH release was significantly (P less than 0.005) greater (about 5-fold). We conclude that the mechanisms which regulate the release and/or biosynthesis of dynorphin and other proenkephalin B-derived peptides of the adenohypophysis are similar to those of the gonadotropins but different from those of any other anterior pituitary hormone, and may be more closely related with FSH release than LH release. These data support the view that dynorphin of the normal rat adenohypophysis may be localized in at least a subpopulation of gonadotrophs.
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PMID:Release of dynorphin-like immunoreactivity from rat adenohypophysis in vitro during inhibition of anterior pituitary hormone secretion from individual cell types. 288 74

Corticotropin-releasing factor initially stimulates the release of beta-endorphin and dynorphin from rat hypothalamic slices in vitro; with time, in the continued presence of corticotropin-releasing factor, the release of both these peptides declines. The studies described here were undertaken to test whether this decline could be due to the operation of inhibitory feedback mechanisms associated with the function of the opioidergic neurons. When the opioid receptor antagonist naloxone was added to the superfusion medium in the presence of corticotropin-releasing factor, the time-related decrease in opioid release was not observed. Potassium ions also caused an increase, followed by a decrease, in opioid peptide release, and naloxone also prevented the latter from occurring. In addition, naloxone on its own, produced a Ca2+-dependent increase in the non-stimulated release of beta-endorphin and dynorphin, and this action was resistant to tetrodotoxin. These findings suggest that opioid receptors mediate inhibitory feedback effects upon the secretory activity of beta-endorphin and dynorphin neurons in the hypothalamus.
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PMID:Feedback inhibition of opioid peptide release in the hypothalamus of the rat. 289 Oct 81

Somatostatin activates an inwardly rectifying potassium conductance in AtT-20 clonal corticotrophs, a cell line derived from the mouse pituitary gland. The action of somatostatin is blocked by pertussis toxin indicating that a GTP-binding protein couples the somatostatin receptor to the potassium channel. The potassium conductance is depressed by cesium. Cesium also attenuates the suppression of adrenocorticotropin hormone secretion by somatostatin suggesting that the increase in potassium conductance plays a role in this action of somatostatin.
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PMID:A potassium conductance contributes to the action of somatostatin-14 to suppress ACTH secretion. 289 64

The effect of barium and potassium on the secretion and biosynthesis of enkephalin in bovine chromaffin cells, and prolactin and beta-endorphin in rat anterior pituitary cells, was examined to determine whether calcium-dependent secretion and biosynthesis are mediated by the same or by different calcium targets within the neuroendocrine cell. In the presence of 1.8 mM calcium, barium and potassium stimulated the secretion of all three peptides over 30 min, and increased the levels of proenkephalin and prolactin mRNA in 24 hr. These effects were inhibited by the calcium channel blocker D600. When the extracellular calcium concentration was lowered to 0.1 mM or less, secretion elicited by potassium was blocked, whereas secretion elicited by barium was enhanced, indicating that barium wholly substitutes for extracellular calcium in mediating peptide secretion. On the other hand, stimulation of proenkephalin and prolactin mRNA by both potassium and barium was inhibited when the extracellular calcium concentration was reduced. We conclude that calcium acts at two different intracellular targets to activate secretion versus biosynthesis of both enkephalin and prolactin. This appears to be the first report in which two different calcium-dependent processes in the intact cell are distinguished by a calcium ion agonist. Calcium-dependent processes such as protein phosphorylation, protein translocation, and enzyme activation may thus be related to events in the intact cell such as peptide synthesis and secretion on the basis of selective stimulation by barium.
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PMID:Barium distinguishes separate calcium targets for synthesis and secretion of peptides in neuroendocrine cells. 295 45

An in-vitro superfusion system was used to study the effects of the endogenous opioid peptides [Met]-enkephalin (and its long-lasting analogue [D-Ala2,Met]-enkephalinamide), [Leu]-enkephalin and beta-endorphin and of the opiate antagonist naloxone, on the secretion of LHRH from the mediobasal hypothalamus of the cockerel. The effects of the compounds on both basal release of LHRH and on release stimulated by a depolarizing pulse of increased extracellular potassium ion (64 mmol/l) were investigated. None of the endogenous opioid peptides altered basal release of LHRH; however, both [Met]-enkephalin (10 mumol/l) and [D-Ala2,Met]-enkephalinamide (1 mumol/l) significantly (P less than 0.05) reduced the response to depolarization. Neither [Leu]-enkephalin nor beta-endorphin (0.1-10 mumol/l) were effective. Naloxone (1 mumol/l) administered alone significantly (P less than 0.05) increased basal release of LHRH and abolished the inhibitory effects of [Met]-enkephalin and [D-Ala2,Met]-enkephalinamide on depolarization-induced release. These results suggest that the endogenous opioid peptides exert a tonic inhibitory influence on LHRH secretion by the mediobasal hypothalamus of the cockerel.
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PMID:Modulation by endogenous opioid peptides of the secretion of LHRH from cockerel (Gallus domesticus) mediobasal hypothalamic tissue. 295 76

A possible dopaminergic regulation of hypothalamic proopiomelanocortin (POMC)-containing neurons has been investigated in rats by means of in vivo and in vitro approaches. Acute or 3-weeks chronic in vivo treatments with the dopaminergic agonists apomorphine (1 mg/kg: s.c.) and 2-Br-alpha-ergocriptine (2.5 mg/kg; s.c.) or the dopaminergic antagonist haloperidol (0.15-3 mg/kg; i.p.) had no significant effect on the concentration of alpha-melanocyte-stimulating hormone (alpha-MSH) in two hypothalamic regions: arcuate nucleus (AN) and dorsolateral area (DLH). In the same way, chronic administration of the dopaminergic agonists or antagonist did not induce any change in hypothalamic contents of beta-endorphin, another peptide derived from POMC. Reverse-phase high-performance liquid chromatographic analysis revealed that acetic acid extracts of AN and DLH both contained two major forms of alpha-MSH-like peptides: deacetylated alpha-MSH and authentic alpha-MSH. The ratio between these two forms was not altered after acute haloperidol treatment (3 mg/kg, i.p.). The possible effect of dopamine on the release of hypothalamic alpha-MSH was studied in vitro using perifused rat hypothalamic slices. Infusion of dopamine (10(-7)-10(-5)M) or its antagonist haloperidol (10(-5)M) had no effect on spontaneous alpha-MSH release from hypothalamic tissue. In addition, none of these drugs had any effect on potassium (50 mM)-induced alpha-MSH release. It is concluded that dopaminergic neurons are not involved in the regulation of synthesis, post-translational processing (acetylation) or release of hypothalamic alpha-MSH.
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PMID:Hypothalamic alpha-melanocyte-stimulating hormone (alpha-MSH) is not under dopaminergic control. 296 Apr 24

Immunoreactive and bioactive luteinizing hormone (LH) has been shown to be widely distributed in the rodent central nervous system (CNS), particularly in the hypothalamus. Subcellular localization of this LH in fractions rich in synaptosomes and in vitro release by potassium-induced depolarization suggests that this peptide may act in trans-synaptic neuromodulatory roles. Furthermore, a variety of experiments have proved that this brain-based LH is not of pituitary origin. In the in vitro studies reported here characterization of brain-based LH release, in response to gonadotropin-releasing hormone (GnRH), beta-endorphin, and biogenic amines, was examined. Adult male rats were sacrificed by decapitation, hypothalami removed, quartered, and incubated in Krebs Ringer's Bicarbonate (KRB). High potassium concentration and GnRH induced release of LH from these hypothalamic explants in short-term culture and serotonin significantly inhibited release of LH from these explants. In contrast, however, beta-endorphin, norepinephrine, dopamine, and acetylcholine, agents known to modulate pituitary LH release, had no effect on the release of LH from hypothalamic tissues in vitro. Furthermore, beta-endorphin did not alter potassium-induced release of LH from the hypothalamus. Whereas there are some similarities between LH release from the pituitary and from the CNS, the differences reported here suggest that hypothalamic LH does not simply serve as a supplemental source for LH in the general circulation but more likely subserves an entirely different role(s) than its pituitary counterpart, presumably acting in a neuromodulatory fashion within the brain.
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PMID:In vitro LH release from the hypothalamus-pars tuberalis; effects of gonadotropin-releasing hormone (GnRH), beta-endorphin and biogenic amines. 296 55


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