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

The concentrations of beta-endorphin and cholecystokinin were measured in lymphocytes obtained from young or old rats and from humans at different ages. Both in rats and humans, beta-endorphin and cholecystokinin increase with age; also in vitro, after 48-h culturing, the concentrations of beta-endorphin and cholecystokinin in lymphocytes obtained from humans of different ages changed with the same pattern observed in ex vivo experiments. In the human, beta-endorphin in lymphocytes shows a circadian rhythm that shifts approximately 6 h when compared to plasma ACTH and cortisol rhythm. The HPLC analysis of the molecular forms of beta-endorphin in lymphocytes revealed the presence of N-acetyl-beta-endorphin, with a ratio of beta-endorphin to N-acetyl-beta-endorphin ranging from 1 to 2. The concentrations of beta-endorphin and cholecystokinin were also measured in lymphocytes obtained from rats and human subjects undergoing different pharmacological treatments. In rat, the serotonin receptor antagonist metergoline decreased basal concentrations of the opioid peptide and blocked the increase of beta-endorphin concentrations induced by the serotonin precursor 5-hydroxytryptophan and the tricyclic antidepressant chlorimipramine. Also in the human, the antidepressant drug chlorimipramine increased lymphocyte beta-endorphin concentrations. In contrast to what was observed for beta-endorphin, cholecystokinin concentrations were not affected by the modulation of the serotoninergic system. Chronic treatment of rats with the dopamine receptor antagonist haloperidol induced an increase of beta-endorphin concentrations in lymphocytes that was reversed by the concomitant treatment with the dopamine receptor agonist bromocriptine, which when given alone decreased the basal concentrations of the peptide. In the human, haloperidol increased concentrations of beta-endorphin after both 24 h and chronic treatment, while cholecystokinin was never affected. Finally, beta-endorphin, but not cholecystokinin, increases both in rat and human lymphocytes after treatment with the GABA agonist sodium valproate.
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PMID:Effect of psychoactive drugs on lymphocyte neuropeptides. 214 59

The neuropeptide beta-endorphin is present in cells of the immune system, i.e., lymphocytes and monocytes, and its expression can be induced by immunological stimuli. In the present study, we showed that the increase of the serotoninergic availability induces an increase of beta-endorphin concentrations in rat peritoneal macrophages that is blunted by the administration of serotonin receptor antagonists. A significant increase of beta-endorphin concentrations is also evident after blocking the dopaminergic receptors, whereas a dopaminergic agonist decreases the concentrations of the peptide. Our data are consistent with a similar modulation of beta-endorphin concentrations in central nervous system and in immune cells, e.g., rat peritoneal macrophages.
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PMID:Pharmacological modulation of beta-endorphin in rat peritoneal macrophages. 253 52

Adrenergic and perhaps dopaminergic neurons provide inhibitory regulation of growth hormone (GH) secretion in ruminants. This suggests that either serotonergic or other neurons regulate the stimulatory release of GH. The nature of neurotransmitter control of adrenocorticotropin (ACTH) secretion in ruminants has not been determined. Parachlorophenylalanine (PCPA; serotonin synthesis inhibitor), quipazine (serotonin receptor agonist) and cyproheptadine (serotonin receptor antagonist) were utilized in Holstein steers to determine whether serotonin receptors mediate stimulatory actions on GH and ACTH secretion. PCPA (100 mg/kg BW) administered each day at 1900 hr for three successive days did not alter mean GH concentrations, amplitude of GH peaks, nor the number of GH peaks. Likewise, PCPA altered none of these parameters for ACTH. Quipazine injected iv at .1 or .5 mg/kg BW increased plasma GH (P less than .05) and ACTH (P less than .001) concentrations. There was a dose effect of quipazine on both GH (P less than .05) and ACTH (P less than .0001) secretion. Pretreatment of steers with cyproheptadine (.06 and .6 mg/kg BW) reduced the stimulation of GH by quipazine (P less than .0001) and decreased basal GH concentrations (P less than .0004). Cyproheptadine at .06 mg/kg BW did not alter quipazine effects on ACTH, however, the higher dose decreased the peak ACTH response (P less than .02) to quipazine. Studies with quipazine and cyproheptadine indicated that serotonergic mechanisms are likely involved in the regulation of GH and ACTH secretion in steers.
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PMID:Effects of parachlorophenylalanine, quipazine and cyproheptadine on growth hormone and adrenocorticotropin secretion in steers. 285 63

A specific radioimmunoassay was used to measure immunoreactive dynorphin (ir-DYN) and beta-endorphin (ir-BE) in the brain, pituitary and gut, following a pharmacological manipulation of the serotonin system. Administration of the serotonin receptor agonist m-chlorophenylpiperazine (m-CPP, 2.5-5 mg/kg ip) or the serotonin releasing agent fenfluramine (20-40 mg/kg ip) induced a significant increase in the hypothalamic ir-BE content and a decrease in its anterior pituitary level. These effects were antagonized by cyproheptadine (1 mg/kg ip). Similar results were obtained after fluvoxamine (15 mg/kg ip), femoxetine (10 mg/kg ip) and 5-hydroxytryptophan (5-HTP 40-160 mg/kg ip). None of the above treatments altered significantly the ir-DYN content in the brain and pituitary. However, the gut ir-DYN level was dramatically decreased after m-CPP, fenfluramine, fluvoxamine, femoxetine and 5-HTP. The latter effect was antagonized by cyproheptadine. The obtained results suggest that serotonergic activation stimulates the release of beta-endorphin from the anterior pituitary and dynorphin from the gut, while the cerebral beta-endorphin system appears to be inhibited by activation of serotonin neurons.
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PMID:Serotonergic regulation of the brain and gut beta-endorphin and dynorphin content in the rat. 287 Apr 87

Serotonin and dopamine neurons have been shown to exert a stimulatory and inhibitory control, respectively, over pituitary release of beta-endorphin-like immunoreactivity (beta-END-LI). In the present study we sought to determine whether an interaction exists between these two reciprocal mechanisms regulating beta-END-LI in the rat. The intraperitoneal (i.p.) administration of 5 mg/kg quipazine, a serotonin receptor agonist, or 2.5 mg/kg haloperidol, a dopamine receptor antagonist, each elevated circulating levels by beta-END-LI 5-fold over control levels by 30 min post-injection. Pretreatment (1 h) with 5 mg/kg, i.p., cinanserin, a serotonin receptor antagonist, completely blocked the quipazine-induced rise in beta-END-LI without affecting the elevated levels of beta-END-LI in haloperidol-treated animals. Conversely, pretreatment (2 h) with 1 mg/kg, i.p., bromocriptine, a dopamine receptor agonist, had no effect on quipazine-induced release of beta-END-LI but did completely prevent the rise in plasma beta-END-LI due to haloperidol treatment. Gel filtration chromatography revealed that quipazine and haloperidol treatments elevated plasma levels of both beta-END-size immunoreactivity and beta-lipotropin (beta-LPH)-sized immunoreactivity though to different relative degrees. However, since circulating levels of beta-LPH serve as a marker for anterior lobe (AL) beta-END-LI secretion, serotonin and dopamine appear to exert stimulatory and inhibitory control, respectively, over AL beta-END-LI release. Further, the quipazine-induced rise in total plasma beta-END-LI primarily resembled beta-LPH in size and was blocked by cinanserin but not bromocriptine pretreatment. And conversely, bromocriptine but not cinanserin prevented the haloperidol-induced rise in circulating beta-END-LI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serotonin and dopamine independently regulate pituitary beta-endorphin release in vivo. 300

A pharmacological approach was used to investigate serotonergic control of the secretion of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) in the rat. The administration of 75 or 200 mg/kg L-tryptophan (ip, over 30 min) increased brain serotonin by 17% and 19%, respectively, and increased circulating beta-END-LI from 0.30 +/- .06 to 0.56 +/- 0.7 and 0.64 +/- 0.8 ng/ml, respectively. D,L,5-Hydroxytryptophan (30 mg/kg, ip, over 30 min) produced a 4.9-fold increase in brain serotonin content and a 3.4-fold rise in plasma beta-END-LI. The administration of a serotonin reuptake blocker, fluoxetine (10 mg/kg, ip, over 15 min), elevated basal levels of plasma beta-END-LI from a control value of 0.38 +/- 0.02 to 1.21 +/- 0.32 ng/ml. Exposure to ether increased circulating beta-END-LI to 1.08 +/- 0.18 ng/ml, and fluoxetine treatment further increased this rise to 1.69 +/- 0.09 ng/ml (P less than 0.05). Quipazine, a serotonin receptor agonist, evoked a dose-related (2.5-5.0 mg/kg, ip) increase in circulating beta-END-LI levels by 15-45 min post injection. By contrast, intraventricular injection of the neurotoxin 5,7-dihydroxytryptamine (75 microgram free base, for 10 days) caused a 77% depletion of brain serotonin and attenuated the rise in beta-END-LI levels in response to immobilization (3.28 +/- 0.20 vs. 1.83 +/- 0.25 ng/ml). A higher dose of 5,7-dihydroxytryptamine (200 microgram free base, for 10 days) significantly decreased resting levels of beta-END-LI from 0.65 +/- 0.14 to 0.36 +/- 0.08 ng/ml. We conclude that brain serotonin neurons exert a stimulatory influence over the basal secretion of pituitary beta-END-LI and mediate, in part, the stress-induced release of this hormone.
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PMID:Evidence that a serotonergic mechanism stimulates the secretion of pituitary beta-endorphin-like immunoreactivity in the rat. 626 89

Cyproheptadine and its metabolite desmethylcyproheptadine were shown to suppress directly the release of adrenocorticotrophin (ACTH) and beta-lipotrophin/beta-endorphin activity from the neurointermediate lobe of the pituitary gland incubated in vitro. Neither compound affected the release of ACTH from the anterior pituitary gland. Serotonin stimulated the release of ACTH and beta-lipotrophin/beta-endorphin activity from the neurointermediate lobe, but did not influence the (desmethyl)cyproheptadine-mediated inhibition of hormone release. These results indicate that serotonin and cyproheptadine affect hormone release by the neurointermediate lobe by a direct action. The effect of cyproheptadine, however, might not be exerted by a serotonin receptor.
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PMID:Cyproheptadine and desmethylcyproheptadine directly inhibit the release of adrenocorticotrophin and beta-lipotrophin/beta-endorphin activity from the neurointermediate lobe of the rat pituitary gland. 630 Feb 74

Using gel filtration chromatography (Sephadex G-50) and radio-immunoassay for beta-endorphin (beta-END) and beta-lipotropin (beta-LPH) we investigated the site [anterior lobe (AL) vs. intermediate lobe (IL)] for serotonergic control of pituitary beta-END-like immunoreactivity (beta-END-LI) in the rat. Since the secretion of beta-LPH in vitro clearly distinguishes beta-END-LI release by the AL as compared to the IL, we interpreted changes in plasma levels of immunoreactivity resembling beta-LPH to reflect beta-END-LI release from the AL. Following the administration of L-tryptophan (200 mg/kg, 30 min, ip), a serotonin precursor, nearly all of the rise in total plasma beta-END-LI was due to the form of immunoreactivity resembling beta-LPH in molecular size. Similarly, 5-hydroxytryptophan (30 mg/kg, 30 min, ip), a serotonin precursor, and fluoxetine (10 mg/kg, 15 min, ip), a serotonin reuptake blocker, predominantly increased circulating levels of beta-LPH-sized immunoreactivity with little effect on beta-END-sized immunoreactivity. Quipazine (2.5 and 5.0 mg/kg, 30 min, ip), a serotonin receptor agonist, elevated plasma levels of both forms of beta-END-LI; however, the immunoreactive peak coeluting with beta-LPH was primarily affected, being increased 9.5-fold while that resembling beta-END was increased less than 1-fold. Immobilization stress (30 min) dramatically elevated plasma levels of both forms of immunoreactivity, however, a greater relative rise in beta-LPH than beta-END was observed. Intraventricular administration of 5,7-dihydroxytryptamine (75 micrograms, free base, 10 d), a serotonin neurotoxin, lowered plasma levels of both forms of immunoreactivity about equally in stressed animals. Further, dexamethasone, a synthetic glucocorticoid which selectively inhibits AL corticotroph secretion in vitro, attenuated the beta-LPH response to serotonergic activation in vivo. Together, these findings indicate that serotonergic drugs predominantly influence the release of beta-END-LI resembling beta-LPH and further suggest that serotonin neurons preferentially regulate the release of beta-END-LI from AL corticotrophs in vivo.
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PMID:Evidence for serotonergic stimulation of pituitary beta-endorphin release: preferential release from the anterior lobe in vivo. 630 75

Fear (i.e., decreased percentage time spent on open-arm exploration) in the elevated plus-maze can be potentiated by prior inescapable stressor exposure, but not by escapable stress. The use of fear-potentiated plus-maze behaviour has several advantages as compared to more traditional animal models of anxiety. (a) In contrast to the traditional (spontaneous) elevated plus-maze, which measures innate fear of open spaces, fear-potentiated plus-maze behaviour reflects an enhanced anxiety state (allostatic state). This "state anxiety" can be defined as an unpleasant emotional arousal in face of threatening demands or dangers. A cognitive appraisal of threat is a prerequisite for the experience of this type of emotion. (b) Depending on the stressor used (e.g., fear of shock, predator odour, swim stress, restraint, social defeat, predator stress (cat)), this enhanced anxiety state can last from 90 min to 3 weeks. Stress effects are more severe when rats are isolated in comparison to group housing. (c) Drugs can be administered in the absence of the original stressor and after stressor exposure. As a consequence, retrieval mechanisms are not affected by drug treatment. (d) Fear-potentiated plus-maze behaviour is sensitive to proven/putative anxiolytics and anxiogenics which act via mechanisms related to the benzodiazepine-gamma-aminobutyric acid receptor, but it is also sensitive to corticotropin-releasing receptor antagonists and glucocorticoid receptor antagonists and serotonin receptor agonists/antagonists complex (high predictive validity). (e) Fear-potentiated plus-maze behaviour is very robust, and experiments can easily be replicated in other labs. (f) Fear-potentiated plus-maze behaviour can be measured both in males and females. (g) Neural mechanisms involved in contextual fear conditioning, fear potentiation and state anxiety can be studied.Thus, fear-potentiated plus-maze behaviour may be a valuable measure in the understanding of neural mechanisms involved in the development of anxiety disorders and in the search for novel anxiolytics. Finally, the involvement of corticotropin-releasing factor and corticosteroid-corticotropin-releasing factor interactions in the production of fear-potentiated plus-maze behaviour are discussed.
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PMID:A robust animal model of state anxiety: fear-potentiated behaviour in the elevated plus-maze. 1260 Jul 8

Neuroendocrine responses to administration of serotonin releasing agents or 5-hydroxytryptamine (5-HT) 1A receptor agonists have been used as an index of serotonin receptor function in patients with depression and other mood disorders. However, the receptor population that mediates these responses has not been clearly identified. We tested the hypothesis that 5-HT1A receptors in the paraventricular nucleus of the hypothalamus (PVN) mediate the release of adrenocorticotropin hormone (ACTH) and oxytocin after administration of a selective 5-HT1A agonist in conscious rats. Low-dose infusion (1 nmol/100 nl/side) of the selective 5-HT1A antagonist, WAY100635 (WAY; [O-methyl-3H]-N-(2-(4-(2-methoxyphenyl)-1-piperazinyl) ethyl)-N-(2-pyridinyl)cyclohexanecarboxamidetrihydrochloride), into the PVN blocked the rise in ACTH and oxytocin stimulated by low-dose (30 nmol/kg) i.v. administration of the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 274 +/- 53 versus 70 +/- 20 pg/ml, P < 0.01 for ACTH and 10.7 +/- 3.4 versus 4.6 +/- 0.7 pg/ml, P < 0.05 for oxytocin after saline or WAY pretreatment, respectively). WAY did not influence the bradycardic effect of 8-OH-DPAT (-56 +/- 7 versus -54 +/- 6 beats per minute after saline or WAY). 8-OH-DPAT treatment also elicited locomotor activation followed by hind limb abduction and flat body posture. Surprisingly, WAY attenuated some aspects of locomotor activation and reduced the duration of hind limb abduction elicited by the agonist (5.1 +/- 0.9 versus 0.3 +/- 0.3 min for saline- or WAY-treated rats). These data indicate that 5-HT1A receptor stimulation in the PVN mediates the characteristic neuroendocrine response to serotonin agonist challenge. Moreover, they provide the first evidence that aspects of the behavioral serotonin syndrome are mediated by forebrain hypothalamic receptors.
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PMID:5-Hydroxytryptamine 1A receptors in the paraventricular nucleus of the hypothalamus mediate oxytocin and adrenocorticotropin hormone release and some behavioral components of the serotonin syndrome. 1574 27


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