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PubMed1982

The effects of des-enkephalin-gamma-endorphin and des-Tyr1-a-endorphin on regional serotonin metabolism in rat brain.

Des-enkephalin-gamma-endorphin (beta-endorphin6-17; DE gamma E) causes a significant reduction of the serotonin concentration of the raphe area of the mesencephalon and of the dorsal hippocampus of the rat. DE gamma E does not, however, alter the pargyline-induced accumulation of serotonin in either of these two brain regions or in the mediobasal hypothalamus. Des-Tyr1-a-endorphin (beta-endorphin2-16; DTaE), on the other hand, inhibits the accumulation of serotonin following MAO-inhibition by pargyline in all 3 brain regions, while, in addition to causing a transient reduction in the serotonin concentration of the raphe area, it decreases the serotonin concentration of the mediobasal hypothalamus. These results indicate that DE gamma E and DTaE, which have been shown to exert opposite effects on behavior in various behavioral tests, both affect regional serotonin metabolism in rat brain and that they do so differently.

Animals↗
PubMed1984

gamma-Endorphin and N alpha-acetyl-gamma-endorphin interfere with distinct dopaminergic systems in the nucleus accumbens via opioid and non-opioid mechanisms.

Low doses (10 ng) of the dopamine agonist apomorphine induced hypolocomotion when injected into the nucleus accumbens of rats. This behavioral response was antagonized by local treatment with either the opioid peptide gamma-endorphin (gamma E) or the non-opioid peptide N alpha-acetyl-gamma-endorphin (Ac gamma E) in a dose of 100 pg. High doses of apomorphine (10 micrograms) r amphetamine (2 micrograms) injected into the nucleus accumbens resulted in hyperlocomotion. This response was blocked by pretreatment with gamma E but not with Ac gamma E. This effect of gamma E could be prevented by local treatment with naloxone. Neither peptides interfered with the apomorphine-induced stereotyped sniffing when the substances were injected into the nucleus caudatus. It is concluded that gamma E and Ac gamma E differentially interact with distinct dopaminergic systems in the nucleus accumbens of the rat brain via an opioid and a non-opioid mechanism, suggesting that the peptide fragments originating from pro-opiomelanocortin may be specifically implicated in the control of dopaminergic activity in this brain area.

Animals↗
PubMedDate not supplied

Chronic ethanol treatment decreases specific nonopiate beta-endorphin binding to hepatic and kidney membranes and lowers plasma beta-endorphin in the rat.

In a previous study we reported the presence of specific nonopiate beta-endorphin (BE) binding sites in peripheral tissues of the rat (Dave JR, Rubinstein N, Eskay RL: Evidence that beta-endorphin binds to specific receptors in rat peripheral tissue and stimulates the adenylate cyclase-adenosine 3',5'-monophosphate system. Endocrinology 117:1389-1396, 1985). The objective of this study was to determine the effect of chronic ethanol administration in vivo on specific nonopiate binding of BE in hepatic and kidney membranes. Experimental animals were exposed continuously for 14 days to ethanol vapor in an inhalation chamber at vapor levels sufficient to maintain blood ethanol levels greater than 120 mg/100 ml, whereas control animals were maintained in ethanol-free chambers. Chronic ethanol treatment decreased [125I]BE binding to hepatic and kidney membranes by approximately 35%, which was due to a decrease in the number of BE binding sites. Chronic ethanol treatment decreased immunoreactive BE in plasma by greater than 80%. In vitro exposure of hepatic and kidney membranes from control animals to ethanol resulted in a dose-related enhancement of BE binding with maximal enhancement of 50-65% being observed at 0.2% ethanol concentration. In contrast, the addition of ethanol in vitro to hepatic and kidney membranes derived from rats chronically exposed to ethanol in vivo did not affect BE binding. Our findings demonstrate that chronic alcohol exposure lowers immunoreactive BE in plasma and reduces BE binding in hepatic and kidney membranes. The observed reduction of BE binding may be due to ethanol-induced changes in membrane composition.

Alcoholism↗
PubMed1981

Effect of intraventricular beta-endorphin and morphine on hypothalamic-pituitary-adrenal activity and the release of pituitary beta-endorphin.

The effects of intraventricular (i.v.t.) morphine sulfate (MS) and beta-endorphin (beta-EP) on pituitary-adrenal activity and the release of pituitary beta-EP were studied in rats. Pituitary-adrenal activity was monitored by measuring plasma corticosterone (CS) levels. 45 min after i.v.t. injection, both MS and beta-EP caused dose-related increases in plasma CS, with beta-EP being approximately ten times more potent on a molar basis. MS injected i.v.t. at 0.3, 1.0, 3.0 and 10.0 microgram did not cause a significant reduction in pituitary immunoreactive (i.r.) beta-EP, but did cause an increase in plasma i.r. beta-EP at 3 microgram of MS. beta-EP injected i.v.t. at 1.5 microgram caused a reduction of pituitary i.r. beta-EP. Since i.v.t.-injected beta-EP may have contributed to the measured plasma i.r. beta-EP, a nonimmunoreactive analog (Des-Asn20-beta c-EP) was used to assess the change in plasma i.r. beta-EP. 5 microgram of DES-Asn20-beta c-EP injected i.v.t. caused increases in plasma i.r. beta-EP and CS, as well as a 40% reduction in pituitary i.r. beta-EP. The concomitant intraperitoneal (i.p.) injection of naloxone HCl (10 mg/kg) significantly blocked the increase in plasma CS induced by 5 microgram of beta-EP. When naloxone HCl, 10 mg/kg was injected alone, a significant increase in plasma CS was found. The results indicate that i.v.t. beta-EP is more potent than MS in causing the release of pituitary ACTH and beta-EP. These findings are consistent with a role for brain endorphins in the regulation of CRF release.

Animals↗
PubMed1986

[Maternal beta-endorphin secretion during pregnancy--measurement of immunoreactive beta-endorphin in urine].

Gestational variations in maternal beta-endorphin (beta-end) secretion were investigated by simultaneous measurements of plasma and urinary immunoreactive beta-endorphin (ir-beta-end). Urinary ir-beta-end was extracted by using a Sep-Pak C18 column and was found to be stable for at least 24 hours at room temperature. Plasma and urine (2 hour collection) samples were obtained from 41 pregnant women and 7 non-pregnant women. Almost parallel increases in plasma and urinary ir-beta-end were observed during the course of pregnancy and there was a good correlation between them. Compared with non-pregnant values, significant increases (p less than 0.001) were observed after 36 weeks of gestation. We also studied chromatographic patterns of urinary extracts of non-pregnant and pregnant women. Both of them consist of 4 peaks and resemble each other. They were essentially similar to those of plasma extracts except for the third peak which appeared between the elution position of beta-lipotropin (beta-LPH) and beta-end. In conclusion, maternal beta-end secretions increase in late gestation not only in plasma but also in urine.

Adult↗
PubMed1990

Localisation of acetylcholinesterase in rat myotubes in the presence of beta-endorphin and beta-endorphin-(1-27).

In rat embryo skeletal myotubes, acetylcholinesterase is present, as multiple forms, and can be detected in deposits at the cell surface. Myotubes cultured in the presence of beta-endorphin, exhibit an increased predominance of the globular (precursor) forms of the enzyme, which are largely restricted to intracellular sites associated with nuclei. In the presence of beta-endorphin-(1-27), the relative proportions of the different forms of acetylcholinesterase is similar to that seen in the controls, but the enzyme is intracellular and has a characteristic focal localisation in the myotube.

Acetylcholinesterase↗
PubMed1982

Effect of des-Tyr1-gamma-endorphin and des-Tyr1-alpha-endorphin on alpha-MPT-induced catecholamine disappearance in rat brain nuclei: a dose--response study.

The effect of des-Tyr1-gamma-endorphin (beta-LPH62-77, DT gamma E) and des-Tyr1-alpha-endorphin (beta-LPH62-76, DT alpha E), administered intracerebroventricularly (icv) in doses of 0.01, 0.1, 1 and 10 micrograms, was studied on the alpha-methyl-p-tyrosine-(alpha-MPT) induced disappearance of catecholamines in a number of microdissected rat brain regions, which were selected on the basis of the neuroanatomy of the dopamine systems in the brain and of previous observations. A dose-dependent increase in the disappearance of dopamine in alpha-MPT-pretreated rats was observed following icv administration of DT gamma E in the nucleus interstitialis striae terminalis, the paraventricular nucleus, the anterior hypothalamic nucleus and the zona incerta. In these same brain regions a decrease in the alpha-MPT-induced disappearance of dopamine was found following the administration of DT alpha E, but only after doses of 0.01, 0.1 and 1 microgram. In none of these regions were effects observed after 10 micrograms of DT alpha E. No effects were seen on dopamine utilization in the nucleus accumbens, caudate nucleus and median eminence after any of the doses of DT gamma E or DT alpha E. The alpha-MPT-induced disappearance of noradrenaline was significantly enhanced in the anterior hypothalamic nucleus of rats treated with DT gamma E. It is concluded that DT gamma E and DT alpha E induce opposite changes in the utilization of dopamine selectively in brain regions which are predominantly innervated by neurons belonging to the intradiencephalic dopamine systems.

Animals↗
PubMed1991

Endoproteolytic conversion of beta-endorphin-1-31 to beta-endorphin-1-27 potentiates its central cardioregulatory activity.

Brain neurons that express the pro-opiomelanocortin gene secrete multiple forms of beta-endorphin (beta E) which subserve diverse bioregulatory processes. beta E-1-31, for example, is a potent analgetic but beta E-1-27 acts as an opioid antagonist and beta E-1-26, as well as the N-acetyl derivatives of all 3 peptides, lack opioid receptor activity. The present study examines the effects of beta-endorphin processing on its central cardioregulatory potency. Consistent with previous reports, intracisternal beta E-1-31 (1.5 nmol) injection lowered mean arterial pressure (MAP); MAP was reduced by 29.7 +/- 3.9 mm Hg at 60 min and returned toward baseline by 120 min. Unexpectedly, beta E-1-27 displayed a 10-fold greater hypotensive potency than beta E-1-31. At 0.15 nmol, it produced a response equivalent to 1.5 nmol beta E-1-31 while 1.5 nmol beta E-1-27 sustained a maximal reduction in MAP (49.2 +/- 3.9 mm Hg) throughout the 120-min test period. In contrast, beta E-1-26 and N-acetyl-beta E-1-26, -1-27 and -1-31 were inactive at 1.5 nmol. Bradycardia accompanied the depressor response to the higher beta E-1-27 dose but not to beta E-1-31. Naloxone pretreatment completely blocked the depressor effects of both beta E-1-31 and beta E-1-27, and reversed the bradycardia produced by beta E-1-27, suggesting that both peptides act through opioid receptors. beta E-1-27 also stimulated catecholamine release from the perfused adrenal gland but beta E-1-31 was inactive. These findings emphasize the importance of regionally selected post-translational processing in defining the functional specificity of beta E peptides.

Adrenal Glands↗
PubMed1982

Electroencephalographic changes in the lateral septum complex following systemic administration of des-Tyr1 -alpha-endorphin, des-Tyr1-gamma-endorphin and haloperidol in rats.

The influence of systemically administered Des-Tyr1-alpha-endorphin (DT alpha E), Des-Tyr1-gamma-endorphin (DT gamma E) and haloperidol on electroencephalographic (EEG) activity of the lateral septum complex (LSC) and the frontal cortex was studied in male rats. DT alpha E (2 micrograms) significantly increased whereas DT gamma E (10 micrograms) significantly decreased the amounts of activity in the 5 Hz band. In addition, DT alpha E promoted production of 15-20 Hz activity, while DT gamma E decreased the amount of 20-30 Hz activity. EEG activity exhibited a marked variability which persisted throughout the recording session following administration of the peptides. Haloperidol markedly decreased the proportion of 10-15 Hz activity. The alterations in EEG of the frontal cortex were similar to those in LSC but less pronounced. The differences in the time course and frequency bands affected suggest that the effects of peptides and haloperidol on EEG activity of LSC are not mediated by the same mechanisms.

Animals↗
PubMed2001

Synthetic beta-endorphin-like peptide immunorphin binds to non-opioid receptors for beta-endorphin on T lymphocytes.

The synthetic decapeptide H-SLTCLVKGFY-OH (termed immunorphin) corresponding to the sequence 364-373 of the CH3 domain of human immunoglobulin G heavy chain was found to compete with [125I]beta-endorphin for high-affinity receptors on T lymphocytes from the blood of healthy donors (K(i) = 0.6 nM). Besides immunorphin, its synthetic fragments H-Val-Lys-Gly-Phe-Tyr-OH (K(i) = 15 nM), H-Leu-Val-Lys-Gly-Phe-Tyr-OH (K(i) = 8.0 nM), H-Cys-Leu-Val-Lys-Gly-Phe-Tyr-OH (K(i) = 3.4 nM), H-Thr-Cys-Leu-Val-Lys-Gly-Phe-Tyr-OH (K(i) = 2.2 nM), H-Leu-Thr-Cys-Leu-Val-Lys-Gly-Phe-Tyr-OH (K(i) = 1.0 nM) possessed the ability to inhibit specific binding of [125I]beta-endorphin to T lymphocytes. Tests of the specificity of the receptors revealed that they are not sensitive to naloxone and Met-enkephalin, i.e. they are not opioid receptors. K(d) values characterizing the specific binding of 125I- labeled immunorphin and its fragment H-Val-Lys-Gly-Phe-Tyr-OH to the receptors have been determined to be 7.4 nM and 36.3 nM, respectively.

Amino Acid Sequence↗
PubMed2001

The content of beta-endorphin-like immunoreactivity in porcine corpus luteum and the potential roles of progesterone, oxytocin and prolactin in the regulation of beta-endorphin release from luteal cells in vitro.

The amount of beta-endorphin-like immunoreactivity (beta-END-LI) in porcine corpora lutea from several stages of the oestrous cycle and the effects of progesterone, oxytocin, and prolactin on beta-END-LI secretion in vitro by luteal cells were studied. Porcine corpora lutea obtained on days 1-5, 6-10, 11-13, 14-18, and 19-21 of the cycle were used to prepare extracts for beta-END-LI determination. Additionally, corpora lutea from days 11-13 and 14-18 were enzymatically dissociated and isolated luteal cells were used for further study of beta-endorphin secretion in vitro. Cells were cultured in serum-free defined M 199 medium (106 cells/ml) at 37 degrees C under 5% CO2 in air, for 12 h. The influences of the following factors on beta-END-LI secretion by luteal cells were tested: progesterone (10-9, 10-7 and 10-5 M), oxytocin (0.01, 0.1, 1 and 10 ng/ml), and prolactin (0.1, 1, 10 and 100 ng/ml). The beta-END-LI contents in extracts and media were measured by radioimmunoassay. The tissue concentration of beta-END-LI was lowest on days 1-5 of the cycle (0.35 +/- 0.03 ng/g wet tissue). Subsequently, it constantly increased to the highest value on days 14-18 (16.58 +/- 0.52 ng/g wet tissue) and on days 19-21 it declined (11.10 +/- 0.52 ng/g wet tissue). Progesterone at a low dose (10-9 M) resulted in significant (p < 0.05) increases and decreases in beta-END-LI secretion by luteal cells from days 11-13 and 14-18, respectively. Higher doses of progesterone (10-7 and 10-5 M) had no effect on beta-END-LI release, compared with the control group. All dose-levels of oxytocin used decreased beta-END-LI secretion by luteal cells on days 11-13 and 14-18 of the cycle. Prolactin at doses of 0.1 and 1 ng/ml on days 11-13, and all doses tested on days 14-18 resulted in decreases in beta-END-LI release from luteal cells. These results document evident changes in beta-END-LI content in the pig corpus luteum during its development and indicate the potential roles of progesterone, oxytocin, and prolactin in luteal cell secretion of beta-END-LI.

Animals↗
PubMed1978

[Antigenic determinants of beta-LPH, beta-MSH, alpha-endorphin, ACTH and alpha-MSH revealed by anti-beta-endorphin in neurons of the human infundibular nucleus].

Comparison of adjacent serial sections of the tubero-infundibular region of Human adult hypothalamus demonstrates that the same perikarya, axons and terminals are stained both with anti-beta-endorphin and anti 17-39 ACTH antisera. The most immunoreactive of these neurons are also revealed with anti alpha-endorphin, anti alpha and beta-MSH, anti-1-24 ACTH and anti beta-LPH. These results suggest that neurons of the infundibular nucleus can store and probably secrete peptide similar to propiocortin or fragment(s) of this molecule.

Adrenocorticotropic Hormone↗
PubMed1984

Non-opiate beta-endorphin fragments and dopamine--VI. Behavioural analysis of the interaction between gamma-type endorphins and dopaminergic systems in the nucleus accumbens of rats.

Injection of small doses of apomorphine, bromocriptine and the new ergoline compound, GYKI-32887 into the nucleus accumbens decreased locomotor activity when rats were tested in a small open field. This effect was observed following injection of 1 pg of these substances; GYKI-32887 being more potent than bromocriptine. The hypolocomotion induced by the ergoline compound could be prevented by local pretreatment with haloperidol (30 pg), fluphenazine (30 pg), sulpiride (10 pg) or desenkephalin -gamma-endorphin (DE gamma E; 100 pg). Large doses of apomorphine and amphetamine, injected into the nucleus accumbens, increased locomotor activity. This behavioural response was antagonized by pretreatment with haloperidol (30 pg), but not with sulpiride (10 pg) or DE gamma E (100 pg or 10 ng). It is concluded that two dopaminergic receptor systems exist in the nucleus accumbens with different sensitivity to apomorphine. One of these receptor systems, which is activated by small doses of apomorphine and ergoline compounds, can be blocked by classical and atypical neuroleptics and by the neuroleptic-like peptide DE gamma E. This may be of relevance to the antipsychotic action of these substances.

Amphetamine↗
PubMed1985

Identification and secretion of gamma-endorphin and beta-endorphin-like peptides from the neurointermediate pituitary of the rat.

Gamma-endorphin (gamma E) and related peptides were chromatographically identified in extracts of neurointermediate (NIL) pituitary. When extracts of this tissue were purified and subjected to HPLC in order to identify gamma E-related peptides gamma E, des-tyrosine gamma E, des-enkephalin-gamma E, and alpha-N acetyl gamma E co-elutable peptides were evident. Perifusates of dispersed NIL tissue were also shown to contain beta E and gamma E-immunoreactivity, and the secretion of both was suppressed by exposure of the tissue to dopamine. This study provides evidence of the endogenous presence and secretion of pharmacologically active gamma E-related peptides by the intermediate lobe of the rat pituitary.

Animals↗
PubMed1976

Isolation, primary structure, and synthesis of alpha-endorphin and gamma-endorphin, two peptides of hypothalamic-hypophysial origin with morphinomimetic activity.

The isolation and primary structure of two peptides with morphinomimetic activity, obtained from an extract of porcine hypothalamus-neurohypophysis, are described. The amino acid sequence of the two peptides, named alpha-endorphin and gamma-endophin, was determined by mass spectrometry and danxyl-Edman methods to be H-Tyr-Gly-Gly-Phe-Met-Thr-Ser-Glu-Lys-Ser-Gln-Thr-Pro-Leu-Val-Thr-OH and H-Tyr-Gly-Gly-Phe-Met-Thr-Ser-Glu-Lys-Ser-Gln-Thr-Pro-Leu-Val-Thr-Leu-OH, respectively. These correspond to the amino acid sequences present between residues 61 and 76 and residues 61 and 77 of the various beta-lipotropins. A third peptide also obtained in pure form in these studies was found to be an unstable salt of alpha-endorphin.

Amino Acid Sequence↗
PubMed1985

Influence of early beta-endorphin treatment on the behavior and reaction to beta-endorphin in the adult male rat.

A study was made of the influence of early exposure to beta-endorphin (beta-END) on the adult behavior and response to beta-END in male rats. beta-END was given during a neonatal period, at 1-5 days of age (1 microgram/animal/day s.c.). Recordings of the development of home-nest-orientation ability, body weights, and sex-specific approach behavior showed that the early beta-END treatment did not have debilitating or other non-specific effects. The early beta-END treatment did cause significant changes in the establishment of the adult pattern of sex-specific approach behavior. Copulatory behavior was not apparently influenced. Intracerebroventricular injection of beta-END (1 microgram) at an adult age induced changes in exploratory and copulatory behaviors and in the pattern of sex-specific approach behavior. The reaction to this treatment with respect to components of socio-sexual behavior differed significantly between males treated early with beta-END and their corresponding controls. No differences were observed in behaviors in the exploratory test situation. It is concluded that early beta-END treatment in rats influences components of socio-sexual behavior and the response to exogenous beta-END in adulthood.

Animals↗
PubMed1984

beta-Endorphin-induced analgesia is inhibited by synthetic analogs of beta-endorphin.

Competitive antagonism of human beta-endorphin (beta h-EP)-induced analgesia by synthetic beta h-EP analogs with high in vitro opiate receptor binding to in vivo analgesic potency ratio has been demonstrated. A parallel shift of the dose-response curve for analgesia to the right was observed when either beta h-EP or [ Trp27 ] -beta h-EP was coinjected with various doses of [Gln8, Gly31 ]-beta h-EP-Gly-Gly-NH2, [Arg9,19,24,28,29]-beta h-EP, or [ Cys11 ,26, Phe27 , Gly31 ]-beta h-EP. It was estimated that the most potent antagonist, [Gln8, Gly31 ]-beta h-EP-Gly-NH2, is at least 200 times more potent than naloxone.

Analgesia↗
PubMed2002

beta-Endorphin-like peptide SLTCLVKGFY is a selective agonist of nonopioid beta-endorphin receptor.

It has been found that beta-endorphin (beta-END) and a synthetic beta-END-like decapeptide Ser-Leu-Thr-Cys-Leu-Val-Lys-Gly-Phe-Tyr (termed immunorphin, IMN) corresponding to the sequence 364-373 of human IgG heavy chain stimulate Con A-induced proliferation of T lymphocytes from the blood of healthy donors. [Met(5)]enkephalin ([Met(5)]ENK) and an antagonist of opioid receptors naloxone (NAL) tested in parallel were not active. The stimulating effect of beta-END and IMN on T lymphocyte proliferation was not inhibited by NAL. Studies on receptor binding of (125)I-labeled IMN to T lymphocytes revealed that it binds with high affinity to NAL-insensitive binding sites (K(d) = 7.0 +/- 0.3 nM). Unlabeled beta-END completely inhibited the specific binding of (125)I-labeled IMN to NAL-insensitive binding sites on T lymphocytes (K(i) = 1.1 +/- 0.2 nM). Thus, beta-END and IMN bind to common NAL-insensitive binding sites on T lymphocytes and enhance Con A-induced proliferation of these cells.

Amino Acid Sequence↗