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Biomedical subjects

C Gianoulakis

Publications and source records attributed to C Gianoulakis.

At least 55 records · Page 3Linked to original sources
PubMed1988

The effect of electroconvulsive therapy on endorphins in depression.

The time course study of the endorphin response to electroconvulsive therapy (ECT) was carried out in 10 patients (including one control who did not receive active ECT) at the first and sixth ECT. Results showed a significant rise of plasma endorphin levels after ECT. This increase returned to the pre-ECT level within 1 hr after ECT. There was a pre-rise of plasma endorphin level, which probably was stress related and which was also observed in the control case.

Depressive Disorder↗
PubMed1988

Effects of ethanol withdrawal on beta-endorphin levels in rat brain and pituitary.

Rats which received a liquid diet containing 6.5% (w/v) ethanol for three weeks became tolerant to the hypothermic effect of an acute dose of ethanol. Withdrawal of this diet was followed by loss of the tolerance within 3 days, and by an accompanying pattern of changes in levels of immunoreactive-ir-beta-endorphin in several brain regions. An initial decrease in levels on days 1 and 3 of withdrawal was followed by recovery to control levels on days 8 and 15. This pattern was found in the arcuate nucleus, amygdala, septum, periventricular thalamus and pre-optic periventricular hypothalamus (POPH), but was statistically significant only in the POPH. A different pattern of change in ir-beta-endorphin levels was found in the pituitary. The anterior lobe showed a significant depletion of ir-beta-endorphin levels before alcohol withdrawal, which recovered by day 8 of withdrawal. This depletion was probably not related to the loss of tolerance to ethanol but was a response to a perturbation of the hypothalamic-pituitary axis of hormonal control.

Animals↗
PubMed1988

Effects of ethanol treatment and withdrawal on biosynthesis and processing of proopiomelanocortin by the rat neurointermediate lobe.

Male Sprague Dawley rats were chronically pair-fed with liquid diets containing 6.5% (vol/vol) ethanol, or equicaloric sucrose. After 21 days the ethanol-containing diet was discontinued and both groups were fed the sucrose diet. Groups of animals were killed on day 22 (0 day of ethanol withdrawal) and 1, 3, 8, and 15 days after ethanol withdrawal and the neurointermediate lobes (NILs) were removed and incubated with [3H]phenylalanine for 3 h. Chronic ethanol treatment induced an increase in the biosynthesis and release of beta-endorphin-like peptides by the rat NIL. After ethanol withdrawal the beta-endorphin-like immunoreactivity content in the NIL and the in vitro release of immunoreactive beta-endorphin (beta EP) by the NIL were significantly lower than in the controls on the first day, whereas no significant difference was found on days 3, 8, and 15 after ethanol withdrawal. The in vitro incorporation of [3H]phenylalanine into POMC, beta-lipotropin and beta EP was found to be higher in the ethanol-treated animals than in the controls on days 0, 1, and 3 after ethanol withdrawal, with no significant difference on days 8 and 15 after ethanol withdrawal. Furthermore, in both the ethanol-treated animals and their pair-fed controls the rate of incorporation of [3H]phenylalanine into total proteins, POMC, beta-lipotropin, and beta EP was significantly higher on days 8 and 15 after ethanol withdrawal than on the day of ethanol withdrawal (day 0), suggesting the implication of a nutritional factor. HPLC analysis of the beta EP peptides indicated that the percentage of acetylated forms of beta EP was higher in the NIL of the alcohol-treated animals, especially on days 8 and 15 after ethanol withdrawal. This observation suggests that though the rates of biosynthesis and release of beta EP-related peptides have returned to normal at 15 days after ethanol treatment, the activity of the enzyme responsible for the acetylation of beta EP remained elevated.

Acetylation↗
PubMed1987

Effect of acute ethanol in vivo and in vitro on the beta-endorphin system in the rat.

Acute ethanol treatment in vivo (i.p. injection of 3.5 g ethanol/Kg B. wt.) stimulated the release of beta-endorphin like peptides by the pituitary gland as was indicated by the increased content of beta-endorphin like immunoreactivity (beta-EPLIR) in the plasma. Furthermore, a significant decrease in the anterior lobe content of beta-EPLIR was observed, while the decrease in the neurointermediate lobe beta-EPLIR content at 45 min after the i.p. ethanol injection was not statistically significant. In vitro incubation of neurointermediate lobes, from animals injected with either ethanol or saline, in the presence of 3H phenylalanine indicated that the content of beta-EPLIR in the incubation medium was increased, the content of the newly biosynthesized 3H-phenylalanine labelled proteins in the neurointermediate lobe extract was decreased, while the content of 3H-phenylalanine labelled pro-opiomelanocortin, beta-lipotropin and beta-endorphin in the neurointermediate lobes extract were not significantly changed by the ethanol treatment, though a small increase was observed. When neurointermediate lobes from untreated control animals were incubated for 3 hrs with 3H-phenylalanine in the presence or absence of 300 mg ethanol per 100 ml incubation medium, there was no significant difference in the beta-EPLIR content in the incubation medium, or in the content of 3H-phenylalanine labelled proteins, pro-opiomelanocortin, beta-lipotropin and beta-endorphin in the neurointermediate lobe extract. These results suggest that ethanol has little or no direct effect on the beta-endorphin peptides in the pars intermedia cells.

Animals↗
PubMed1987

The beta-endorphin response to stress during postnatal development in the rat.

The plasma beta-endorphin and adrenocortical responses to ether and handling stress were examined in animals of various ages. At each age studied there was a significant, stress-induced elevation of plasma beta-endorphin-like immunoreactivity levels. Moreover, basal beta-endorphin-like immunoreactivity levels were higher in animals 3, 7, and 14 days of age than in adults. In contrast, plasma corticosterone levels in the Day 7 pups were not elevated by stress; a finding consistent with several previous reports on the absence of increased release of adrenocorticotropin and corticosterone during stress in the neonate. These data suggest that the release of adrenocorticotropin and beta-endorphin in response to stress differ in the developing animal.

Animals↗
PubMed1987

Effect of prenatal exposure to ethanol on body growth and the pituitary beta-endorphin.

Pregnant rats were fed an ethanol diet from the first day of pregnancy until parturition. Control rats were either pair fed with an isocaloric sucrose diet, or fed with standard lab chow (basic control group). Rats fed with the ethanol diet and their pair-fed controls showed a similar increase in body weight during pregnancy, which was lower than the increase observed in the basic control group. At 10 days after ethanol withdrawal all three groups presented similar body weights. A lower body growth was exhibited by the offspring of both the ethanol and the sucrose pair-fed rats, implicating a prenatal nutritional factor on the postnatal growth. Furthermore, the rate of body growth was lower in the offspring of the ethanol-treated animals than in the offspring of both their pair-fed and the basic control rats, indicating the presence of an additional ethanol-associated factor. On day 4 of development, the concentration of beta-endorphin peptides (pmol/mg protein) in the pituitary gland and the anterior lobe, of the offspring of the ethanol-treated animals and their sucrose pair-fed controls, was significantly higher than that of the offspring of the basic control animals. However, a lower content of beta-endorphin-like peptides was noticed in the whole pituitary gland, the anterior lobe, and the intermediate lobe of the offspring of the ethanol-treated rats and their pair-fed controls on days 8, 14, and 22 postnatally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Inbred strains of mice with variable sensitivity to ethanol exhibit differences in the content and processing of beta-endorphin.

The content of beta-endorphin-like immunoreactivity (beta-EPLIR) in the anterior and neurointermediate lobe of the pituitary gland, the hypothalamus and the serum of the c57BL/6, BALB/C and DBA/2 inbred strains of mice was estimated at the resting state as well as 45 min after i.p. injection of either ethanol solution (3.0 g/kg.b.wt.) or saline. At the resting state, the neurointermediate lobe and the serum of the c57BL/6 mice showed the highest content of beta-EPLIR, while no statistically significant difference was noticed in the total beta-EPLIR content in the anterior lobe and hypothalamus. At 45 min post-ethanol treatment the beta-EPLIR content was increased in the serum of all three strains of mice studied and was decreased in the hypothalamus of the c57BL/6 mice only. Further analysis of the beta-endorphin peptides using sephadex G-75 chromatography and reverse phase high performance liquid chromatography indicated strain differences in the relative proportions of the various forms of beta-endorphin in the anterior lobe, neurointermediate lobe and the hypothalamus. These strain specific differences in the content and post-translational processing of beta-endorphin may be involved in some of the genetically determined differences in responses to ethanol by these inbred strains of mice.

Animals↗
PubMed1986

Neurointermediate lobe transplanted under the kidney capsule modifies the activity of the neurointermediate lobe in situ, but does not respond to opiate treatment.

To investigate the possibility of a direct effect of morphine on the pars intermedia cells of the pituitary gland, rat neurointermediate lobes (NIL) were transplanted under the kidney capsule. At 2 and 8 days posttransplantation the NIL transplant had maintained its morphological integrity. However, at 15 days posttransplantation the morphological integrity of the NIL transplant had started to deteriorate. The NIL transplant contained, synthesized, and released beta-endorphin-like peptides. It was noticed that there was very little beta-endorphin in the radiolabelled biosynthesized products, suggesting that either the maturation processing of proopiomelanocortin was modified, or that beta-endorphin was released immediately as soon as it was formed and did not accumulate in the tissue. In support of the latter possibility was the elevated content of beta-endorphin-like immunoreactivity in the sera of rats with a NIL under the kidney capsule. Furthermore, the NIL transplant seemed to produce a substance or substances which could decrease the content, the biosynthesis and the release of beta-endorphin-like peptides by the NIL in situ. Treatment with either morphine or naloxone for 5 days did not change the beta-endorphin-like immunoreactivity content in the NIL transplanted under the kidney capsule. However, a distinct decrease in the beta-endorphin-like immunoreactivity in the NIL in situ of animals with or without a NIL transplant was observed following the morphine treatment. Naloxone treatment induced a decrease in the beta-endorphin-like immunoreactivity content in the hypothalamus, but had no effect on the beta-endorphin-like immunoreactivity content in the anterior lobe and NIL of the pituitary gland in situ or in the NIL transplant.

Animals↗
PubMed1986

Effect of maternally administered opiates on the development of the beta-endorphin system in the offspring.

Pregnant rats received subcutaneous implantation of either morphine or placebo pellets at various stages of gestation. Untreated animals served as basic controls. The effect of morphine treatment on the growth of the offspring as well as on the ontogeny of beta-endorphin in the pituitary gland and the hypothalamus was investigated. Results obtained indicated that pregnant rats treated with morphine from day 1 of pregnancy to day 21 presented complete resorption. Subcutaneous implantation of a morphine pellet on days 11, 13 and 19 of gestation allowed pregnancy to term, however the post-natal mortality rate was very high. Implantation of a morphine pellet on days 9 and 13 of gestation allowed pregnancy to term and after birth the withdrawal reaction of the offspring was mild and the mortality rate was low. At early stages of development there were differences in the pituitary and hypothalamic beta-endorphin content between the offspring of the morphine treated animals and the offspring of the control animals, but by day 22 no significant differences among the various groups were noticed.

Aging↗
PubMed1985

Endorphins in inbred mice with variable sensitivity to ethanol: effect of acute ethanol treatment.

Resting levels of beta-endorphin like immunoreactivity were determined in the hypothalamus, neurointermediate lobe and anterior lobe of the pituitary gland and the serum of inbred mice strains (C57BL/6, BALB/C and DBA/2). C57BL/6 mice showed the highest content of beta-endorphin like immunoreactivity in the neurointermediate lobe, anterior lobe and serum. Animals were injected i.p. with either an ethanol solution (3g ethanol/Kg b. wt.) or saline. 45 minutes post ethanol treatment the beta-endorphin like immunoreactivity content was increased in the serum of all three strains of mice studied and was decreased in the hypothalamus of the C57BL/6 mice. Studies with reverse phace HPLC indicated some differences in the relative proportions of the various forms of beta-endorphin in some tissues among the three strains of mice. These results suggest that genetically determined differences in endorphin levels may be involved in some of the genetically determined differences in responses to ethanol.

Animals↗
PubMed1983

Long-term ethanol alters the binding of 3H-opiates to brain membranes.

In order to examine whether ethanol treatment has selective or differential effects on brain binding sites for opiates, male Sprague Dawley rats were fed for 15 or 21 days with a complete liquid diet containing 6.5% ethanol (v:v) or an isocaloric amount of sucrose. The binding of 3H-DADL-enkephalin, 3H-dihydromorphine and 3H-naloxone to the brain membranes from rats treated with ethanol was increased. However, addition of ethanol directly in the incubation medium decreased the binding of 3H-DADL enkephalin and increased the binding of 3H-dihydromorphine to brain membranes from both control and ethanol treated rats. Direct exposure of brain membranes to ethanol caused no significant change in the binding of 3H-naloxone. Thus chronic ethanol ingestion alters the binding of opiate ligands to brain membranes. Furthermore, the direct effect of ethanol appears to be different for the different classes of opiate binding sites.

Animals↗
PubMed1983

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.

Animals↗
PubMed1981

Effect of chronic morphine treatment on beta-endorphin biosynthesis by the rat neurointermediate lobe.

The effect of chronic morphine treatment on the in vitro biosynthesis of beta-endorphin by rat pars intermedia was investigated. Tolerance and physical dependence were induced in 200 g rats by the subcutaneous implantation of 75 mg morphine pellets for either 3 days or 15 days. Immediately following sacrifice of the animals the neurointermediate lobes were removed and incubated with [3H] phenylalanine. The protein extracts of the lobes were analyzed for the incorporation of the labelled amino acid into total protein, pro-opiomelanocortin, beta-lipotropin (beta-LPH) and beta-endorphin. the biosynthesized products were purified by immunoprecipitation with an antiserum to beta-endorphin. The identity and purity of beta-endorphin were verified by polyacrylamide disc gel electrophoresis with sodium dodecyl sulfate, and microsequencing. The identity of pro-opiomelanocortin (POMC) was verified by peptide mapping of its tryptic digestion products. The results showed that morphine treatment induced a decrease in the incorporation of the radioactive amino acid into total protein, pro-opiomelanocortin, beta-LPH and beta-endorphin. The decrease was more pronounced for the incorporation into beta-LPH and beta-endorphin than into pro-opiomelanocortin and total proteins, suggesting an effect of morphine treatment on the processing of the pro-opiomelanocortin to its final maturation products.

Amino Acids↗
PubMed1980

Rat beta-LPH, gamma-LPH and beta-endorphin biosynthesized by isolated cells of pars intermedia and pars distalis. Further characterization.

Rat pars intermedia cells were incubated for 3 h with the following amino acids: (a) 35S-methionine and 3H-phenylalanine, (b) 3H-valine; and (c) 3H-valine and 3H-lysine. Radioactive gamma-lipotropin, beta-lipotropin and beta-endorphin were purified on carboxymethyl-cellulose and characterized by polyacrylamide disc gel electrophoresis at pH 4.5, molecular weight estimation and micro-sequencing. Rat gamma-lipotropin was shown to differ slightly from ovine gamma-lipotropin in its NH2-terminal amino acid sequence, in containing no methionine and having phenylalanine at position 6, valine at positions 13 and 27, and lysine at position 20. The same variations were observed in the sequence of rat beta-lipotropin, while rat beta-endorphin was shown to be identical to the ovine beta-endorphin. Following a 3-h pulse of rat pars distalis, the cells were extracted with care to avoid beta-lipotropin degradation by proteolytic enzymes, A peptide was purified and identified to be rat beta-endorphin, thus demonstrating that beta-endorphin is biosynthesized in pars distalis and is not an extraction artifact.

Amino Acid Sequence↗
PubMed1980

Chemical characterization of adrenocorticotropin and a novel peptide biosynthesized from a pituitary adenoma of a patient with Cushing's disease.

ACTH and another unidentified peptide have been biosynthesized in vitro and purified from a pituitary adenoma of a patient with Cushing's disease. The new peptide had an apparent molecular weightof 4000 daltons and was more acidic than ACTH as analyzed by sodium dodecyl sulfate/urea and acidic (pH 4.5) polyacrylamide gel electrophoreses, respectively. Sequence studies revealed the presence of [35S]methionine at position 3 of the new peptide. High performance liquid chromatographic analysis of [35S]methionine-labeled tryptic fragments of the peptide revealed that this peptide contained gamma MSH- (1-7) within its sequence. Our observations raise the possibility that this peptide contains at its N-terminus gamma MSH, a putative peptide proposed by Nakanishi et al.

Adenoma↗