Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol (2.0-5.0 g/kg, IP) caused a dose-related impairment of the aerial righting reflex of mice 60 min after injection. Ethanol (3.5 g/kg, IP) given simultaneously with neurotensin (30 micrograms, IC), bombesin (30 micrograms, IC) or beta-endorphin (20 micrograms, IC) caused a greater impairment of the reflex than ethanol alone. Simultaneous treatment with ethanol (4.0 g/kg, IP) and thyrotropin-releasing hormone (TRH, 3.0-30 micrograms, IC) caused less impairment of this measure than ethanol alone. None of the peptides altered the height of aerial righting when administered alone, or when administered with ethanol no peptide altered blood or brain ethanol content. Unexpectedly, TRH (20 and 40 mg/kg, IP) potentiated the action of ethanol by increasing punished licking in water-deprived rats, rather than antagonizing this acute action of ethanol. Like ethanol (1.0 and 2.0 g/kg, IP), beta-endorphin (100 micrograms, IC) suppressed ethanol-withdrawal tremor and audiogenic-seizure susceptibility in ethanol-dependent rats. beta-Endorphin (1 microgram) and bombesin (10 and 30 micrograms, IC) reduced only audiogenic-seizure susceptibility. TRH (10-100 micrograms, IC, or 1-40 mg/kg, IV) and neurotensin (10-100 micrograms, IC) had no effect on these ethanol-withdrawal signs. These findings suggest that centrally active peptides may play a role in certain acute and chronic actions of ethanol. Because TRH, neurotensin, bombesin and beta-endorphin do not alter all actions of ethanol in the same way, an interaction of ethanol with many functionally independent neuronal circuits is suggested.
 ...
PMID:Modification of the actions of ethanol by centrally active peptides. 626 62

Tolerance to ethanol was induced in male Sprague-Dawley rats (225-250 g) by chronic feeding with a liquid diet containing 6.5% ethanol (v/v). Control rats were pair-fed with a liquid diet in which the ethanol was replaced by an equicaloric concentration of sucrose. Immediately following sacrifice of the animals the neurointermediate lobes (NIL) were removed and incubated with [3H]phenylalanine. The biosynthesized proopiomelanocortin (POMC), beta-lipotropin (beta-LPH), and beta-endorphin (beta-EP) were purified by immunoprecipitation with an antiserum to beta-EP and analyzed by sodium dodecyl sulfate polyacrylamide disc gel electrophoresis. Alcohol treatment for 3 days had no effect on the degree of incorporation of [3H]phenylalanine into POMC, beta-LPH, and beta-EP but treatment for either 15 or 21 days increased the incorporation of [3H]phenylalanine into all three peptides. Ethanol treatment also increased the beta-endorphinlike immunoreactivity (beta-EPLIR) found in the incubation medium, but no significant change was observed in the beta-EPLIR extracted from the NIL either immediately after sacrifice or after 3 h of incubation of the NIL. However, a significant decrease of beta-EPLIR was found in the anterior lobes of rats treated with ethanol for 21 days. Furthermore, the beta-EPLIR in the serum of alcohol-treated rats was significantly higher than in the serum of their corresponding controls. These results indicate an effect of ethanol on the endorphin system and are consistent with the suggestion that endorphins may be mediators of some of the ethanol effects.
 ...
PMID:Chronic ethanol treatment alters the biosynthesis of beta-endorphin by the rat neurointermediate lobe. 631 10

Resting pituitary levels of beta-endorphin-(beta-EP-IR), ACTH-(ACTH-IR), and alpha-MSH-(alpha-MSH-IR)-like immunoreactive material were found to differ among 16 inbred mouse strains. Hormone levels correlated genetically with severity of withdrawal from ethanol, which also differed among the strains. Ethanol dependence led to reduced pituitary beta-EP-IR in 4 of 5 strains studied. After 24 hr of withdrawal, 3 of those 4 showed elevated pituitary beta-EP-IR. These results are consistent with the hypothesis that genetically-determined difference in pituitary hormone functioning underlie some of the genetically-determined differences in ethanol withdrawal severity.
 ...
PMID:Ethanol dependence and the pituitary-adrenal axis in mice. I. Genotypic differences in hormone levels. 631 50

The activity of single neurons in rat cortex or hippocampus (HPC) was recorded to test two hypotheses: (1) neuronal effects of ethanol are mediated by an endogenous opiate-like mechanism (for example, by release of an endogenous opioid peptide), and; (2) ethanol-induced formation of aldehyde-catecholamine condensation products (tetrahydroisoquinolines; TIQs) might contribute to some acute actions of ethanol. Ethanol and all TIQs were applied to single neurons from multibarrel micropipettes by electroosmosis or pressure. Ethanol most often inhibited neurons of the parietal cortex, while activating most HPC pyramidal neurons. Tetrahydropapaveroline (THP) most often inhibited the spontaneous and glutamate- or acetylcholine (ACh)-induced firing of neurons in both these regions, although some excitations were also seen. In contrast, salsolinol and 7-O-methyl-salsolinol predominantly excited HPC pyramidal neurons, but depressed most parietal cortical neurons. Iontophoretic or SC naloxone usually antagonized the excitatory actions of ethanol, salsolinol and methionine5-enkephalin on HPC pyramidal cells; however, ACh-induced speeding also was antagonized occasionally. Conversely, the antimuscarinic agent scopolamine antagonized the excitatory actions of salsolinol, but not those of met-enkephalin, in some HPC pyramidal cells. These results and those of previous studies show that acutely applied ethanol or salsolinol elicits a region-specific pattern of neuronal effects in brain similar to that previously described for opiates: activity is inhibited in several tested brain areas but excited in hippocampus. Furthermore, these excitatory effects are antagonized by naloxone. However, because of the occasional apparent non-specific effects of naloxone and the puzzling antagonism of the salsolinol-induced excitations by scopolamine, some doubt remains whether the opiate-like actions of these substances can be completely attributed to mediation by opiate receptors.
 ...
PMID:Ethanol and some tetrahydroisoquinolines alter the discharge of cortical and hippocampal neurons: relationship to endogenous opioids. 717 89

In this study we have determined the role of cyclic AMP on the function and differentiation of beta-endorphin (beta-EP) neurons in rat fetal hypothalamic cell cultures. Addition of Bt2cAMP or the cAMP elevating agent, forskolin, in cultures, dose and time dependently increased beta-endorphin secretion. The increased beta-EP secretion after Bt2cAMP or forskolin treatment was associated with proopiomelanocortin gene expression, enhanced neurite growth, and increased neuronal viability. Determination of internucleosomal cleavage of DNA by agarose gel electrophoresis revealed that apoptosis occurred in hypothalamic neurons during the first 6-8 days in culture. Addition of Bt2cAMP during this developmental period inhibited DNA degradation in hypothalamic neurons. Furthermore, incubation with various doses of ethanol, which is known to reduce intracellular levels of Bt2cAMP, increased DNA degradation in these cells. Ethanol-induced DNA degradation was blocked by concomitant incubation with Bt2cAMP. Histochemical identification of apoptotic cells following ethanol and Bt2cAMP treatments further revealed that apoptosis occurred in beta-EP neurons during the developmental period, and that ethanol increased and Bt2cAMP reduced apoptotic beta-EP cell numbers. These results suggest that ethanol neurotoxicity on beta-EP neurons during early neuronal differentiation involves an apoptotic process and that the cAMP signaling system plays an important role in controlling apoptosis and differentiation of the beta-EP neuronal system.
 ...
PMID:Cyclic AMP and ethanol interact to control apoptosis and differentiation in hypothalamic beta-endorphin neurons. 792 2

Alcoholism is a familial disorder with both genetic and environmental determinants. The sons of alcoholic fathers have been documented to have alterations in several neuroendocrine measures. We investigated the ACTH/cortisol response to ovine corticotropin-releasing hormone (oCRH) and ethanol in men with and without a family history of alcoholism. Men were defined as family history positive (FHP) (n = 7) if their father was alcoholic; as family history negative (FHN) (n = 16), if their father was nonalcoholic. Ethanol (0.75 g/kg) or placebo was ingested over 15 min, 1 microgram/kg oCRH was administered, and plasma ACTH/cortisol levels were determined at -20, 0, 15, 30, 60, and 90 min after oCRH. Following placebo, FHP men had lower peak ACTH response to oCRH than did FHN men (12 +/- 2 vs 20 +/- 2 pmol/liter, P = 0.04). In FHN men, plasma ACTH response to oCRH was blunted during the ethanol session compared to the placebo session (13 +/- 1 vs 20 +/- 2 pmol/liter; P = 0.006). In contrast, FHP men had similar ACTH responses to oCRH during ethanol and placebo sessions. Cortisol responses to oCRH were similar in both groups during both sessions. In summary, FHP and FHN nonalcoholic men had different plasma ACTH responses following the administration of oCRH.
 ...
PMID:Adrenocorticotropin responses following administration of ethanol and ovine corticotropin-releasing hormone in the sons of alcoholics and control subjects. 797 91

The effect of ethanol, acetaldehyde, and salsolinol on hypothalamic beta-endorphin secreting neurons is studied by using rat fetal hypothalamic neurons in primary culture. Exposure of these neuronal cells to different concentrations of ethanol (12.5-50 mM) and acetaldehyde (12.5-50 microM) caused a concentration-dependent increase in the secretion of beta-endorphin. Salsolinol (12.5-50 microM) did not cause any significant change in the secretion of beta-endorphin. Ethanol's effect was short-lasting (2 hr). Acetaldehyde's effect on beta-endorphin secretion was greater and longer lasting, as compared with ethanol. Ethanol and salsolinol do not have any effect on cell viability, whereas higher concentrations of acetaldehyde appear to reduce the number of viable cells after 6 hr of treatment. None of the above treatments has any effect on cellular DNA content. These results suggest that ethanol is a potent stimulator of hypothalamic beta-endorphin. These results also show for the first time that ethanol's metabolite acetaldehyde is more potent in stimulating beta-endorphin secretion and may be significant in the ethanol regulated beta-endorphin secretion.
 ...
PMID:Effect of alcohol, acetaldehyde, and salsolinol on beta-endorphin secretion from the hypothalamic neurons in primary cultures. 811 41

The present study was conducted to evaluate and compare effects of the benzodiazepine agonist diazepam, antagonist flumazenil and inverse agonist RO 15-4513 on ethanol-induced changes in beta-endorphin (beta-EN) levels in specific rat brain regions. Male Sprague-Dawley rats (150-200 g) adapted to a 12-hour light:12-hour dark illumination cycle were used in this study. Ethanol (3 g/kg as 22.5% solution in saline), flumazenil (10 mg/kg), RO 15-4513 (10 mg/kg), diazepam (2 mg/kg) or a combination of ethanol (3 g/kg) and flumazenil (10 mg/kg), RO 15-4513 (10 mg/kg) or diazepam (2 mg/kg) were administered intraperitoneally to rats at 7.00 h. Control animals were injected with saline. Animals were sacrificed by decapitation 1 h after injection; the brains were immediately removed; the cortex, hippocampus and hypothalamus were dissected and their beta-EN levels measured by radioimmunoassay. Ethanol administration significantly increased beta-EN levels in the hippocampus and hypothalamus but had no effect on beta-EN levels in the cortex. Similar increases in beta-EN levels in the hippocampus and hypothalamus also occurred following either flumazenil or diazepam. On the other hand, RO 15-4513 significantly increased beta-EN levels in the cortex and hypothalamus. When flumazenil was concurrently administered with ethanol, it completely reversed the ethanol effects in the hippocampus but failed to do so in the hypothalamus. Concurrent administration of RO 15-4513 with ethanol also reversed the ethanol-induced rise of beta-EN in the hypothalamus. However, concurrent administration of diazepam and ethanol did not block the increase in beta-EN levels.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of benzodiazepine agonist, antagonist and inverse agonist on ethanol-induced changes in beta-endorphin levels in specific rat brain regions. 827 56

Ethanol has been shown to enhance the in vitro release of hypothalamic beta-endorphin (beta-EP). In the present study, the pattern of beta-EP release by the hypothalamus of two strains of mice, bred selectively for their preference (C57BL/6) or aversion (DBA/2) to ethanol, was investigated using a tissue perifusion system. The tissues were perifused with 20 mM ethanol for 30 min and the immunoreactive beta-EP content was estimated in perifusates collected every 2 min. Ethanol induced an enhanced release of hypothalamic beta-EP characterized by an initial spike followed by a gradual decrease toward baseline levels in both strains of mice. The ethanol-induced increase in beta-EP release by the hypothalamus of the C57BL/6 mice was more pronounced and longer lasting than that by the hypothalamus of the DBA/2 mice. Similar to beta-EP, an immediate sharp increase of corticotropin-releasing hormone (CRH) release was induced by ethanol which, however, did not present a spike but was maintained significantly higher than spontaneous release for the duration of ethanol exposure. Both ethanol-induced beta-EP and CRH release returned to basal levels within 10 min following removal of ethanol. That beta-EP levels did not remain elevated for the duration of ethanol exposure was not due to tissue depletion of releasable beta-EP pool, since exposure of the hypothalami to 10(-8) M CRH for 10 min, immediately after the perifusion with 20 mM ethanol, resulted in a large increase of beta-EP release. A second ethanol exposure 30 min after the first one did not induce an increase in beta-EP release. However, when the recovery period from the first ethanol exposure was extended to 60 min, a significant increase in the release of hypothalamic beta-EP was observed from the hypothalamus of the C57BL/6 but not of the DBA/2 mice. It is concluded that hypothalamic endorphinergic neurons present a fast, transient increase of beta-EP release in the presence of 20 mM ethanol, and become insensitive to subsequent ethanol exposures for a period of about 60 min. In addition, genetically determined differences exist with regards to the magnitude and duration of the ethanol-stimulated release of beta-EP, as well as on the length of the ethanol nonresponsive period. These differences may explain in part the differences in the voluntary ethanol consumption exhibited by these strains of mice.
 ...
PMID:Effects of single and repeated exposures to ethanol on hypothalamic beta-endorphin and CRH release by the C57BL/6 and DBA/2 strains of mice. 836 33

The present investigation was conducted to evaluate the effects of estradiol on ethanol-induced alterations of beta-endorphin (beta-EN) and met-enkephalin (ME) levels in specific brain regions of ovariectomized rats. Female Sprague-Dawley rats (100-124 g) adapted to a 12-hour light, 12-hour dark illumination cycle were used in these studies. Animals were ovariectomized under pentobarbital anesthesia. After a recovery period of 14 days, ethanol (3 g/kg as 22.5% solution in saline, i.p.), estradiol (50 micrograms/kg in 0.2 ml of olive oil, s.c. in the dorsal neck region), or a combination of ethanol and estradiol were administered to rats at 11:00 h. Control animals were injected intraperitoneally with 2 ml saline and subcutaneously with 0.2 ml olive oil. Animals were sacrificed by decapitation 2 h later. The brains were immediately removed; the cortex, hippocampus, hypothalamus, and midbrain were dissected and their beta-EN and ME levels were measured by radioimmunoassay. Ethanol administration significantly decreased both beta-EN and ME levels in the hypothalamus. Administration of estradiol alone also resulted in a significant decrease in beta-EN and ME levels in the hypothalamus. Additionally, concurrent administration of ethanol and estradiol showed a decrease in the levels of beta-EN and ME in the hypothalamus. Co-administration of ethanol with estradiol also caused a significant decrease in the levels of beta-EN in midbrain. However, ME levels were increased in the midbrain after concurrent administration of estradiol and ethanol. ME levels also increased in the hippocampus and cortex after co-administration of estrogen and ethanol. These results clearly indicate that estradiol significantly alters ethanol-induced effects on beta-EN and ME levels in specific brain regions of ovariectomized rats. The present findings may in part explain sex differences in alcohol effects.
 ...
PMID:Estradiol alters ethanol-induced effects on beta-endorphin and met-enkephalin levels in specific brain regions of ovariectomized rats. 893 Oct 99


<< Previous 1 2 3 4 Next >>