Beta-endorphin-like Immunoreactivity Research Articles

Chronic ethanol treatment alters the biosynthesis of beta-endorphin by the rat neurointermediate lobe.

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.

Plasma immunoreactive beta-endorphin and enkephalin concentration in healthy subjects before and after electroacupuncture.

The involvement of the endogenous analgesia systems in the mechanism of analgesia produced by electrical stimulation of the brain or resulting from certain stressful manipulations seems now well-established. The purpose of the present study was to determine whether acupuncture as a method of peripheral sensory stimulation activates, like central stimulation, the endogenous opiate system. Plasma concentrations of ACTH and the best known endogenous opiates: beta-endorphin, met- and leu-enkephalin, were determined before and after standard electroacupuncture stimulation in healthy volunteers. Acupuncture stimulation resulted in a significant (p less than 0.005) decrease of plasma beta-endorphin-like immuno-reactivity (B-EPLI), but plasma ACTH assayed did not change about 5 minutes after acupuncture. The authors conclude that the reaction of the beta-endorphin system to acupuncture (sensory peripheral) stimulation in humans did not involve pituitary hypersecretion, and suggest that the increase of beta-endorphin binding to the tissue receptor sites seems to be responsible for the peripheral (plasma) B-EPLI decrease after acupuncture.

An investigation into opioid systems in the pregnant rat

The role of opioid peptides during pregnancy and parturition has not been defined. They may function as natural analgesics during parturition. Pain thresholds were tested during pregnancy but, in contrast with a previous study, were found not to change. Plasma Beta-endorphin-like-immunoreactivity (B-ELI) was measured and towards the end of pregrancy a significant increase was recorded. Peptide levels returned to the pre-gestational concentration just prior to parturition. Pituitary B-ELI was also measured and was only significantly raised on the day before expected parturition. These changes add to the evidence that opioid peptides have a physiological function during pregnancy and parturition.

Pituitary beta-endorphin, naloxone, and feeding in several experimental obesities.

The role of beta-endorphin in the development of several obesity syndromes was examined. Adult female hooded rats received ventromedial hypothalamic lesions, dorsolateral tegmental lesions, parasagittal hypothalamic knife cuts, intraventricular 5,7-dihydroxytryptamine, ovariectomy, control surgery, or were deprived to 75% of normal body weight. Dose-dependent suppression of food intake by the opiate antagonist naloxone (0.5, 1.8, 6.8, or 25.0 mg/kg, ip) was measured during once-daily 4-h food access periods. No difference was found among the groups at any dose. Pituitary beta-endorphinlike immunoreactivity (BELI) was substantially decreased in knife-cut rats, but was unaltered by other treatments. Obesity had no effect on BELI. In another experiment, rats made obese by prolonged maintenance on palatable foods had elevated pituitary BELI levels. Feeding mechanisms involving opioid peptides do not appear to be of etiological significance in the syndromes examined.