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)

This study demonstrated morphological changes in glial-like cells of the rat pituitary intermediate lobe during early postnatal development, and a subsequent shift in protein expression from vimentin to GFAP. Vimentin immunoreactivity was detected in the lobe at embryo day 14 and was localized in radially-oriented, bipolar cells whose processes spanned the thickness of the intermediate lobe. At electron microscopical resolution, processes contained intermediate filaments, cell nuclei were indented while secretory vesicles characteristic of the endocrine cells were not found. Vimentin immunoreactive intensity began to decrease at postnatal day 5. By postnatal day 7, vimentin-positive, stellate cells were observed, with few radial processes found by day 10. The intensity of vimentin immunoreactivity decreased through day 25. Within the lobe parenchyma, vimentin was localized in glial-like cells since double-label immunohistochemistry revealed no colocalization of beta-endorphin and vimentin, or fibronectin and vimentin. Dopamine-containing axons were in close apposition to vimentin-positive processes. GFAP immunoreactivity first appeared on postnatal day 20 and, by day 25, stellate cell bodies with three to six extended processes were evident. Cells were primarily distributed in the caudal third of the lobe. The characteristic adult pattern of cell clusters in latero-dorsal and ventral portions of the lobe was fully established by postnatal day 55. The transition from vimentin to GFAP expression and concurrent morphological changes resemble those described for radial glial during cerebral cortical development.
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PMID:Glial-like cells of the rat pituitary intermediate lobe change morphology and shift from vimentin to GFAP expression during development. 855 90

Interleukin 6 (IL-6) and tumor necrosis factor (TNF) are released from the zona glomerulosa of rat adrenal glands. The release of these cytokines from adrenal cells is regulated by interleukin 1 beta (IL-1 beta) and lipopolysaccharide (LPS), which are involved in the immune and inflammatory responses. Adrenocorticotropic hormone (ACTH) and angiotensin II, hormones that regulate the adrenal cortex, likewise regulate release of cytokines from adrenal glands. Dopamine inhibits aldosterone release from the adrenal cortex. Therefore, effects of dopamine on IL-6 and TNF release from rat adrenal zona glomerulosa were investigated. Primary cultures of rat adrenal zona glomerulosa cells were exposed to test agents and IL-6 and TNF release determined by the 7TD1 and WEHI bioassays, respectively. Dopamine increased basal IL-6 release and potentiated IL-6 release stimulated by ACTH, LPS or IL-1 beta. Dopamine inhibited basal and secretagogue-stimulated (LPS and IL-1 beta) TNF release. These effects of dopamine were mediated by D2 receptors because N-0437, a D2 agonist, had effects on TNF and IL-6 release identical to those of dopamine. Therefore, dopamine, through D2 receptors, regulates the release of IL-6 and TNF from adrenal cells. Because TNF and IL-6 regulate adrenal steroid release, these cytokines may serve as autocrine or paracrine mediators of adrenal gland function.
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PMID:Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro. 866 82

The release of catecholamines and cortisol from the perifused adrenal region and caudal vein of the eel (Anguilla rostrata) was compared with the release of 39 amino acids and related compounds. Dopamine, norepinephrine and epinephrine were present in all perifusates of the adrenal region. Dopamine release from the caudal vein exceeded that from the adrenal region, and norepinephrine and epinephrine were not detected. Cortisol was present in the perifusate of the adrenal region but virtually absent in caudal vein perifusate. Of the six substances with known or suspected neurotransmitter function, taurine, aspartate, glutamate, glycine and alanine were present in all or almost all samples from both the adrenal equivalent and the caudal vein. gamma-aminobutyric acid (GABA) was detected in a few samples from either preparation. The release of taurine and phosphoethanolamine may be linked to that of norepinephrine and epinephrine. Adrenocorticotropic hormone (ACTH) enhanced the release of cortisol, aspartate, valine, leucine and ornithine from the adrenal region, but the release appears to be from differing sources or cellular pools. Overall, the study revealed that both the adrenal region and caudal vein release a large number of amino acids and related substances. The caudal vein, and possibly other blood vessels as well, may be a major source of circulating dopamine.
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PMID:Release of amino acids and related compounds from the adrenal equivalent and caudal vein of the eel in vitro. 883 79

In recent years much has become known about the substrates in the brain involved in the regulation of masculine sexual behavior and the involvement of specific neurochemicals in these brain areas. In the present paper the experimental data concerning the involvement of a number of brain areas in sexual behavior are reviewed, in relation to an incentive motivational theory of sexual behavior. The review is restricted to the involvement of opioids and dopamine, of which the role in sexual motivation and behavior is best documented. Opioids in the medial preoptic area (mPOA) impair sexual performance, although the endogenous opioids systems may be quiescent in normal, sexually active rats. Dopamine in the mPOA has a facilitative role in the masculine sexual performance. The corticomedial amygdala is involved in processing of sensory information, especially olfactory stimuli, which are subsequently directed towards the mPOA. Local beta-endorphin infusion interferes with this processing. Endogenous opioids in the ventral tegmental area activate the mesoaccumbens dopamine system and stimulate the sexual motivation. Increased dopamine transmission in the nucleus accumbens correlates with increased sexual motivation and vice versa. The basolateral amygdala plays an essential role in the association of environmental stimuli with reward and therefore in the expression of conditioned sexual motivation. Finally, the reviewed data are integrated and a comprehensive view on the relations between various neural substrates is composed.
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PMID:Regulation of masculine sexual behavior: involvement of brain opioids and dopamine. 886 73

This study shows that perinatal exposure to morphine promotes developmental changes (up to 8 months of life) in the striatum by up-regulating concentrations of substance P and met-enkephalin with changes of prometenkephalin A mRNA expression at the day of birth only. Dopamine metabolism (up to 60 days) is also increased as suggested by the reduced concentrations of dopamine and increased content of 3,4-dihydroxyphenylacetic acid. Tyrosine hydroxylase mRNA expression is selectively reduced only in the substantia nigra by perinatal morphine. Serotonin content is reduced only during the early postnatal days and is unaffected thereafter. Supplementation of naltrexone to morphine-exposed rats prevents monoaminergic and neuropeptidergic changes in the striatum, which directly implicates opioid receptors in the developmental changes caused by morphine. The data suggest that perinatal morphine may inhibit met-enkephalin release, causing accumulation of the peptide without corresponding changes in specific mRNA. Dopamine release may also be increased as indicated by a higher metabolism and consequent reduction of tyrosine hydroxylase mRNA expression in the substantia nigra.
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PMID:Exposure to perinatal morphine promotes developmental changes in rat striatum. 888 80

Opioid peptides and their receptors are present in the placenta of many species. Dopamine plays an important role in the regulation of opioid release in the nervous system and it may play a similar role in placenta since dopamine receptors are also present in this tissue. The aim of the present work was to examine the effect of dopamine on the basal release of rat placental opioids. The effect of several dopamine receptor agonists and antagonists was tested on the release of immunoreactive beta-endorphin and immunoreactive dynorphin from perfused rat placenta fragments. We found that dopamine and apomorphine stimulated the secretion of immunoreactive beta-endorphin in a dose-dependent manner. The selective D1 dopamine receptor agonist (+/-)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride or SKF-38393 reproduced the effect of dopamine while the selective D1 dopamine receptor antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl 1,2,3,4,5-tetrahydro-1 H-benzazepine hydrochloride or SCH-23390, prevented the dopamine- and SKF-38393-induced increase of immunoreactive beta-endorphin secretion. The selective and potent D2 dopamine receptor agonist (+/-)-2-(N-phenylethyl-N-propyl) amino-5-hydroxytetralin hydrochloride or PPHT had no effect on immunoreactive beta-endorphin. Finally, none of the agonists tested had any effect on the in vitro secretion of placental immunoreactive dynorphin. Our results suggest that dopamine affects the basal release of placental opioids in an opioid and dopamine receptor-specific manner, its effect being different from the effect it exerts on beta-endorphin in the rat neurointermediate pituitary lobe.
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PMID:Dopamine affects the in vitro basal secretion of rat placenta opioids in an opioid and dopamine receptor type-specific manner. 896 Aug 64

The effect of perfusion of melanin-concentrating hormone (MCH) or alpha-melanocyte-stimulating hormone (alpha-MSH) (100 ng/microliter) in the ventromedial nucleus (VMN) or medial preoptic area (MPOA) on monoaminergic levels of female rats was measured using microdialysis and HPLC-electrochemical detection. In the MPOA, alpha-MSH raised 5-HIAA concentration, whereas MCH reduced both 5-HT and 5-HIAA. Neither peptide had any effect in the VMN. The opposite effects of the peptides on the serotonergic system might be responsible for their antagonistic or opposite actions previously reported on several CNS functions. Dopamine may mediate the similar effects of the two peptides, because alpha-MSH inhibits dopaminergic release in the MPOA (but not VMN) and MCH tends to follow the same pattern.
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PMID:alpha-Melanocyte-stimulating hormone (alpha-MSH) and melanin-concentrating hormone (MCH) modify monoaminergic levels in the preoptic area of the rat. 914 25

Dopamine negatively regulates POMC gene expression in melanotrophs of the intermediate lobe of the pituitary gland. The dopaminergic receptor involved in this control is the dopamine D2 receptor (D2R). The principal products of the POMC gene in melanotrophs are beta-endorphin and alpha-MSH. POMC is differently processed in the corticotrophs, where it is not regulated by dopamine and it is principally processed into ACTH. Here we show that D2R-deficient mice have increased POMC expression and intermediate lobe hypertrophy. Strikingly, D2R-deficient mice have unexpected elevated ACTH levels with a corresponding increase of corticosteroids and consequent hypertrophy of the adrenal gland. This phenotype is reminiscent of Cushing's syndrome in humans. Interestingly, we show that the elevation in ACTH levels is due to an aberrant processing of POMC in melanotrophs. Indeed, we demonstrate that in addition to controlling POMC gene expression in these cells, dopamine, by modulating the expression of the convertases involved in the cleavage of the POMC prohormone, strictly regulates its processing. These results reveal a key role for dopamine in the control of POMC-derived peptides and furthermore indicate an implication of the dopaminergic system in the genesis of Cushing's syndrome.
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PMID:Absence of dopaminergic control on melanotrophs leads to Cushing's-like syndrome in mice. 971 39

Management of pituitary tumors has improved in the past decade since the introduction of novel therapeutic agents. As a result, several treatment options are now available. Dopamine agonists are the preferred treatment for both symptomatic microprolactinomas and macroprolactinomas; these drugs result in normalization of hormone levels and tumor shrinkage in most treated patients. New formulations (such as cabergoline and parenteral bromocriptine) with prolonged duration of action offer improved compliance with treatment and cure rates. For acromegaly and adrenocorticotropin hormone (ACTH)-secreting, thyroid-stimulating hormone (TSH)-secreting, and nonfunctional adenomas, surgery often results in cure. Octreotide and the long-acting, slow-release somatostatin analogues are effective medical alternatives to or adjuvants for transsphenoidal surgery in patients with growth hormone-secreting and TSH-secreting tumors. No drug treatment is available for symptomatic nonfunctional tumors, and patients with ACTH-secreting adenomas may benefit from cortisol-lowering drugs after surgical failure. Pituitary irradiation may be required after surgery for ACTH-secreting, TSH-secreting, and nonfunctioning tumors; it is less commonly required for acromegaly. Although many pituitary tumors are successfully resected, functional adenomas may not be cured by surgery. As more-effective drugs are introduced for the management of pituitary tumors, more patients with hormone-secreting adenomas are being successfully treated medically.
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PMID:Management of pituitary tumors. 973 86

Dopamine (DA) secreted by tuberoinfundibular dopaminergic (TIDA) neurons in the hypothalamus is the major inhibitory factor controlling prolactin (PRL) secretion from the anterior pituitary. Endogenous opioid peptides (EOPs), mainly the neuropeptide beta-endorphin, have a stimulatory influence on PRL secretion. During the first half of pregnancy in rats, PRL secretion is characterized by two daily surges, the nocturnal surge and the diurnal surge. We tested the hypothesis that EOPs are critical stimulatory factors in regulating the nocturnal PRL surge, possibly via inhibition of TIDA neuronal activity. Naloxone (NAL), an opioid antagonist, was continuously infused (0.2 mg/10 microL/min i.v.) during the expected time of the nocturnal PRL surge in day 8 pregnant rats. Radioimmunoassay (RIA) was used to measure plasma PRL levels, and the immunocytochemical (ICC) staining of Fos/FRA was performed to detect changes in transcriptional activity of neurons in the hypothalamus. ICC of tyrosine hydroxylase (TH), the rate-limiting enzyme for DA synthesis, was performed to visualize TIDA neurons in the arcuate nucleus. The results showed that the nocturnal surge of PRL was markedly delayed and dampened in NAL-treated rats (p < 0.01). The numbers of both Fos/FRA and (Fos/FRA)/TH dual-staining neurons increased in the arcuate nucleus following NAL treatment (p < 0.05 for both comparisons). These data indicate that EOPs are critical stimulatory factors for the nocturnal PRL surge and that the actions of EOPs are partially mediated via decreasing TIDA neuronal activity.
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PMID:Effects of naloxone infusion on nocturnal prolactin secretion and Fos/FRA expression in pregnant rats. 1045 Dec 23


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