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At least 55 records · Page 3Linked to original sources
PubMed1983

Suppressive effect of beta-endorphin on body shaking response to ice water immersion and synergistic action of vasoactive intestinal peptide on beta-endorphin in anesthetized rats.

The effects of beta-endorphin and vasoactive intestinal peptide (VIP) on the body shaking response to ice water immersion were observed in anesthetized rats. Intraventricular injection of beta-endorphin markedly inhibited body shaking, but gamma- and alpha-endorphin and methionine-enkephalin showed only slight or little effect. VIP also suppressed the body shaking. The inhibitory effect of beta-endorphin and VIP was blocked by naloxone. When small doses of beta-endorphin and VIP which could not affect the shaking behavior by themselves were administered simultaneously, significant suppression occurred, indicating potentiation of the effect of beta-endorphin by VIP.

Animals↗
PubMedDate not supplied

Effect of endorphin exposure at weaning on the endorphin and serotonin content of white blood cells and mast cells in adult rat.

Hormonal imprinting takes place perinatally at the first encounter between the developing receptor and its target hormone, resulting in the accomplishment of normal receptor development. In the presence of an excess of target hormone or the absence of it, or an excess of related molecules which can be bound by the receptor, faulty imprinting develops with life-long consequences. In previous experiments neonatal endorphin exposure caused a decrease in endorphin and serotonin content of peritoneal mast cells of adult animals. In the present experiment 25-day-old (weaned) female rats received 2 microg endorphin, and the endorphin as well as serotonin content of adult mast cells and white blood cells was studied by flow cytometry and confocal microscopy. Peritoneal lymphocytes and blood monocytes contained significantly (p<0.01) less endorphin and peritoneal mast cells less serotonin (p<0.07, i.e. of questionable significance) than the untreated control. The results bring attention to the possibility of durable imprinting of differentiating cells later in life and to the durable (possibly life-long) effect of an endorphin excess (perhaps caused by injury) manifested in the change of endorphin and serotonin content of immune cells.

Animals↗
PubMed1984

Quantitation of the endopeptidase activity generating gamma-endorphin from beta-endorphin in rat brain synaptic membranes by a radiometric assay.

gamma-Endorphin is a naturally occurring biologically active peptide that is produced by an endopeptidase activity cleaving its precursor beta-endorphin. This enzyme was termed gamma-endorphin generating enzyme (gamma-EGE). In order to quantitate gamma-EGE activity by means of a simple and sensitive assay two synthetic peptides derived from the sequence surrounding the gamma-EGE cleavage site in beta-endorphin were tested as substrates. One of these peptides Ac-Val-Thr-Leu-Phe-Lys-NHCH3 fulfilled all criteria for a suitable gamma-EGE substrate. The peptide was exclusively cleaved at the correct bond for gamma-EGE upon incubation with brain synaptic membranes, and this cleavage was inhibited by the naturally occurring substrate beta-endorphin. The peptide was insensitive to cleavage by exopeptidases and cathepsin D. Addition of a 14C-labeled methyl group at the lysine residue of this peptide by reductive methylation did not alter its properties as a substrate for gamma-EGE activity. The use of the 14C-labeled peptide allowed sensitive quantitation of its radioactive products after simple separation by hydrophobic chromatography on minicolumns containing polystyrene beads. gamma-EGE activity increased linearly with a protein concentration and incubation time. This assay can be used for reliable quantitation of gamma-EGE activity and permits investigations on the regulation of gamma-endorphin production.

Amino Acids↗
PubMed1984

Evidence that spinal endorphin mediates intraventricular beta-endorphin-induced tail flick inhibition and catalepsy.

Naloxone injected intrathecally had a different effect on the inhibition of the inhibition of the tail flick response produced by beta-endorphin and morphine injected intraventricularly. The intrathecal naloxone completely antagonized the effect of beta-endorphin but had only a very weak effect on morphine. In the same rats the cataleptic response to beta-endorphin was antagonized as well; however no definitive conclusion could be made regarding the antagonism of the morphine-induced catalepsy. The results indicate that spinal endorphin is involved in the production of intraventricular beta-endorphin-induced spinal tail flick inhibition and suggest that intraventricular beta-endorphin and morphine elicit their pharmacological action via the activation of different descending inhibitory systems.

Animals↗
PubMed1982

Non-opiate beta-endorphin fragments and dopamine--III. gamma-Type endorphins and various neuroleptics counteract the hypoactivity elicited by injection of apomorphine into the nucleus accumbens.

The hypoactivity in rats induced by small doses of apomorphine, injected bilaterally into the nucleus accumbens area of the brain, could be antagonized by pretreatment with the neuroleptic-like neuropeptide des-enkephalin-gamma-endorphin (DE gamma E, beta-endorphin 6-17) as well as with the neuroleptic drugs haloperidol, sulpiride and clozapine injected into the accumbens. Dose-response studies revealed that a dose of 100 pg DE gamma E completely inhibited the apomorphine-induced hypomotility. The influence of DE gamma E appeared to be specific for gamma-type endorphins, since alpha-type endorphins were inactive in this respect. Treatment with DE gamma E injected into the accumbens for 4 days resulted in an enhancement of apomorphine-induced hypoactivity. It is concluded that gamma-type endorphins may control the activity of dopaminergic transmission in the nucleus accumbens, a suggestion which may be of significance for the purported neuroleptic-like and antipsychotic action of gamma-type endorphins.

Animals↗
PubMed1984

[125I] Tyr27 beta-endorphin: a radio-iodinated derivative of beta-endorphin for the study of opiate receptors.

Evidence is presented that a new derivative of beta-endorphin, [125I] Tyr27 beta-endorphin, is a suitable ligand for the study of beta-endorphin binding sites in rat brain. The results obtained with this homogeneous mono-iodinated peptide demonstrated high affinity agonist binding sensitive to the presence of sodium and magnesium ion and to guanine nucleotide. Competition experiments using a series of opiates and opioid peptides including shorter forms of beta-endorphin revealed a range of potencies; beta-endorphin 1-31 exhibited the highest affinity. The findings suggest that binding sites that complement the structure of beta-endorphin are present in rat cortex.

Animals↗
PubMed1984

Distribution of immunoreactive beta-neo-endorphin in discrete areas of the rat brain and pituitary gland: comparison with alpha-neo-endorphin.

The distribution of immunoreactive (ir)-beta-neo-endorphin in 101 microdissected rat brain and spinal cord regions as well as in the neurointermediate lobe of pituitary gland was determined using a highly specific radioimmunoassay. The highest concentration of beta-neo-endorphin in brain was found in the median eminence (341.4 fmol/mg of protein). High concentrations of ir-beta-neo-endorphin (greater than 250 fmol/mg of protein) were found in 11 nuclei, including dorsomedial nucleus, substantia nigra, parabrachial nuclei, periaqueductal gray matter, anterior hypothalamic nucleus, and lateral preoptic areas. Moderate concentrations of the peptide (between 100 and 250 fmol/mg of protein) were found in 66 brain nuclei such as the amygdaloid and septal nuclei, most of the diencephalic structures (not including the hypothalamus), and the majority of the medulla oblongata nuclei and others. Low concentrations of ir-beta-neo-endorphin (less than 100 fmol/mg of protein) were found in 21 nuclei, e.g., cortical structures (frontal., cingulate, piriform, parietal, entorhinal, occipital), olfactory tubercle, and cerebellum (nuclei and cortex). The olfactory bulb has the lowest beta-neo-endorphin concentration (21.3 fmol/mg of protein). Spinal cord segments exhibit low peptide concentrations. The neurointermediate lobe of the pituitary gland is extremely rich in ir-beta-neo-endorphin.

Animals↗
PubMed1990

Isoproterenol-stimulated release of beta-endorphin and related peptides from the rat pituitary neurointermediate lobe in vitro: evidence for preferential release of certain molecular forms of beta-endorphin.

The intermediate lobe of the pituitary gland synthesizes the multifactorial precursor molecule pro-opiomelanocortin (POMC), from which, through a process of post-translational enzymatic processing, beta-endorphin-(1-31) (beta E) and a variety of N alpha-acetylated and C-terminally shortened forms of this peptide are generated. Using an in vitro superfusion system, the release of these endorphins from intact rat neurointermediate lobes (NILs) was investigated under basal and isoproterenol (ISO) stimulated conditions. Superfusion of NILs with the beta-adrenergic agonist ISO (30 min pulse) resulted in a rapid, sustained and concentration-dependent stimulation of the release of beta E-like immunoreactivity (beta E-IR) over basal as determined with an antiserum directed against the C-terminus of the beta E- (1-31) sequence (10(-6) M: + 145%; 10(-7) M: + 73%; 10(-8) m: + 41%). The release of N(alpha)-acetylated-endorphin-like immunoreactivity (AcE-IR) was stimulated to a similar extent. These effects of ISO were antagonized by the competitive alpha-adrenoceptor antagonist propranolol in a concentration-dependent manner, indicating the involvement of alpha-adrenoceptors. The beta-related peptides released from the NILs under basal and ISO-stimulated conditions were further characterized, based on their retention times in a reversed-phase HPLC system and their reactivity with specific antisera recognizing respectively the midportion of beta E, the N-terminus of acetylated endorphins, the C-terminus of tau-endorphin (beta E-(1-17); tau E), or the C-terminus of alpha-endorphin (beta E-(1-16); alpha E). In HPLC fractionated superfusates 10 peaks were resolved that reacted with the midportion beta E antiserum. In superfusates collected under basal conditions, three major peaks possessed chromatographical and immunological characteristics of Ac beta E-(1-26), Ac beta E- (1-27) Ac beta E-(1-31). In addition, a prominent peak was found eluting around the retention time of beta E-(1-31), that contained both acetylated and non-acetylated material. Six smaller peaks were observed, with the characteristics of beta E-(1-26) and beta E-(1-27) (these peptides were not resolved with the HPLC system used), Ac tau E, tau E, Aa alpha E, and des-tyrosine-alpha E (DT alpha E), respectively. In superfusates collected during superfusion of NILs with ISO (10(-6) M) all peaks were increased. However, those eluting as beta E-(1-31), beta E-(1-26)/beta E-(1-27), Ac beta E-(1-26) and Ac tau E appeared to be preferentially stimulated.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylation↗
PubMed1992

Measurement of beta-endorphin in human plasma by high-performance liquid chromatography with electrochemical detection: validation of a method employing the simultaneous purification and concentration of beta-endorphin.

The simultaneous purification and concentration of synthetic human beta-endorphin from plasma is described, which when used together with an appropriate isocratic high-performance liquid chromatographic-electrochemical detection (HPLC-ED) system allows the determination of elevated physiological levels of beta-endorphin. Purification of plasma was gained by flash-freezing in liquid nitrogen, acidifying with 100 microliters of trifluoroacetic acid (10%, v/v) per ml of plasma, thawing at 4 degrees C and centrifuging to remove any precipitate. Solid-phase extraction with silica sorbent was utilised, which allowed further isolation of the analyte, a method of concentration and a procedure whereby beta-endorphin could be transferred to the HPLC mobile phase. Silica sorbent demonstrated greater selectivity than C18 for synthetic human beta-endorphin and, in addition, provided improved recovery of this analyte when utilising elution volumes of 500 microliters or less. Proteolytic degradation and heparin-induced high-affinity binding in plasma were shown not to effect the recovery of beta-endorphin if blood was rapidly chilled and plasma quickly obtained, frozen and acidified. Validation of this purification/concentration method using [125I]beta-endorphin demonstrated a recovery of 85.6% which was not jeopardised when concentrating the sample twenty-fold. This provided an increase in the sensitivity of detection, when used in conjunction with HPLC-ED, from 5 ng/ml to 250 pg/ml.

Aprotinin↗
PubMed1993

Alpha,N-acetyl beta-endorphin [1-8] is the terminal product of processing of endorphins in the melanotrope cells of Xenopus laevis, as demonstrated by FAB tandem mass spectrometry.

The major N-terminal acetylated endorphin of the pars intermedia of Xenopus laevis was purified and submitted to fast-atom bombardment tandem mass spectroscopy. The collisionally induced dissociation MS/MS spectrum of the [M+H]+ ion revealed sufficient fragment ions to determine unambiguously the identity of the peptide as alpha,N-acetyl beta-endorphin [1-8], the sequence of which was predicted on the basis of the nucleotide sequence of Xenopus POMC cDNA. The determination was confirmed by showing that the synthetic peptide of this structure had identical FAB tandem mass spectrometric characteristics as the endogenous endorphin. We conclude that alpha,N-acetyl beta-endorphin [1-8] is the terminal product of processing of endorphins in the melanotrope cell of Xenopus laevis.

Animals↗
PubMed1982

Effect of des-Tyr1-gamma-endorphin and des-enkephalin-gamma-endorphin on active and passive avoidance behavior of rats; a dose-response relationship study.

The potency of two beta-endorphin fragments, des-Tyr1-gamma-endorphin (DT gamma E, beta E-(2-17) and des-enkephalin-gamma-endorphin (DE gamma E-(6-17) was compared on extinction of pole-jumping avoidance behavior and on retention of a one-trial step-through passive avoidance procedure. Both peptides facilitated the extinction of pole-jumping avoidance behavior and attenuated passive avoidance behavior. The gamma-type endorphin exhibited an inverted U-shaped dose-response curve on passive avoidance behavior but not on extinction of pole-jumping avoidance behavior. DE gamma E appeared to be approximately three times more potent than DT gamma E on extinction of pole-jumping avoidance behavior but one hundred times more potent on passive avoidance behavior. It is suggested that DE gamma E rather than DT gamma E represents the endogenous neuroleptic-like neuropeptide derived from beta-endorphin.

Animals↗
PubMed1982

Non-opiate beta-endorphin fragments and dopamine--II. beta-Endorphin 2-9 enhances apomorphine-induced stereotypy following subcutaneous and intra-striatal injection.

The non-opiate beta-endorphin (beta E) fragment 2-16 (des Tyr1-alpha-endorphin) enhanced apomorphine-induced stereotyped sniffing in rats, but did not interfere with the hypoactivity elicited by small doses of apomorphine. Structure-activity relationship studies revealed that the active moiety of alpha-endorphin fragments with respect to their potentiating effects on apomorphine-induced stereotyped sniffing resides in the beta E fragment 2-9. Subsequent studies showed that the potentiating influence of beta E 2-9 was dependent on the dose of the peptide and that the interaction between this peptide and apomorphine may be non-competitive in nature. The stereotyped sniffing elicited by apomorphine, injected bilaterally into the striatal area of the brain, was dose-dependently enhanced by intra-striatal pretreatment with beta E 2-9. It is concluded that the influence of alpha-type endorphins and beta E 2-9 on apomorphine-induced behavioural changes, is in some aspects opposite to that of gamma-type endorphins, but may be mediated by quite different mechanisms.

Animals↗
PubMed1983

Multi-dimensional analyses of behavior in mice treated with morphine, endorphins and [des-tyrosine1]-gamma-endorphin.

An investigation was made as to the effects of an intracerebral injection of morphine, endorphins and [des-tyrosine1]-gamma-endorphin (DT gamma E) on spontaneous locomotor activity in mice. This was done by exploiting a newly devised multi-dimensional behavioral analyser with a capacitance system. This apparatus simultaneously recorded nine different degrees of behavior (1/1, 1/2, 1/4, 1/8, 1/16, 1/32, 1/64, 1/128 and 1/256) according to the movement sizes in mice. Within 15 min after injection, gamma-endorphin (5 and 10 microgram), leucine-enkephalin (200 micrograms) and methionine-enkephalin (100 micrograms) produced a significant increase in the 1/1 size of movement. Fifteen to 30 min after injection, the movement patterns induced by morphine (40 micrograms) and DT gamma E (40 micrograms) became similar, although morphine (40 micrograms) caused a significant decrease in the 1/1 and 1/2 sizes of movement. beta-Endorphin (2 micrograms) significantly decreased most of the movement sizes for 30 min compared with saline-treated group. [D-alanine2]-methionine-enkephalinamide (20 micrograms) significantly decreased almost all the movement sizes within 15 min after injection. The significant alteration in the movement sizes induced by morphine and endorphins except for DT gamma E was antagonized by pretreatment with naloxone (1 mg/kg). These results strongly suggest the qualitative difference in the behavioral effects of each of the opioids and nonopioid.

Animals↗
PubMed1978

Endorphins in chronic pain. I. Differences in CSF endorphin levels between organic and psychogenic pain syndromes.

A series of 37 patients with chronic pain was investigated with regard to neurologic and psychiatric variables. Twenty of the patients were classified as having mainly organic (= somatogenic) pain syndromes while 17 patients were rather suffering from psychogenic pain syndromes. Samples of lumbar cerebrospinal fluid (CSF) were obtained from the patients and analyzed for the presence of opiate receptor-active material, here called endorphins. Patients classified as having mainly organic pain syndromes were found to have significantly lower endorphin levels than patients with predominantly psychogenic pain syndromes. In the total group of patients as well as in the two subgroups, there was a significant correlation between CSF endorphin levels and the depth of depressive symptomatology as reported by the patients. On the other hand, there was no correlation between CSF endorphin levels and extent of anxiety or motor retardation. It is concluded that CSF endorphins reflect central processes involved in chronic pain syndromes.

Adult↗
PubMed1981

Beta-Endorphin: synthesis and radioreceptor binding activity of Beta h-endorphin-(1-27) and its analogs.

Beta h-Endorphin-(1-27) (I), [Ac-Tyr1]-beta h-endorphin-(1-27) (II), [Gln8]-beta h-endorphin-(1-27) (III), and [Ac-Tyr1, Gln8]-beta h-endorphin-(1-27) (IV) were synthesized by the solid-phase method. The binding potency of I-IV to rat brain membrane preparations was measured by radioreceptor binding assay. The relative potencies were: beta h-endorphin, 100; I, 30; II, 0.04; III, 90; IV, 0.07.

Amino Acid Sequence↗
PubMed1981

Stress-induced release of brain and pituitary beta-endorphin: major role of endorphins in generation of hyperthermia, not analgesia.

The present paper examines the conjectured causal relationship between the alterations in brain, pituitary and plasma levels of endorphins and the antinociception (analgesia) and hyperthermia elicited by acute stress. A 5-min foot-shock instigated a significant depression in the levels of beta-endorphin immunoreactivity (beta-EI) in both the hypothalamus and periventricular beta-endorphinergic fibre-containing tissue. A large elevation in plasma levels of beta-EI, consisting of about 70% beta-endorphin (beta-EP), and 30% beta-lipotropin (beta-LPH) was associated with a significant reduction in the beta-EI content of both the anterior (AL) and neurointermediate (NIL) lobes of the pituitary. No concomitant changes in the levels of Met-enkephalin immunoreactivity (M-EI) in discrete areas of brain and pituitary were detectable. Application of a high (10 mg/kg) but not a low (1 mg/kg) dose of naloxone, prior to foot-shock, slightly reduced the increase in tail-flick latency evoked by this stress. In contrast, both of these doses strongly and dose-dependently attenuated the accompanying rise in core temperature (Tc). Chronic (approximately 30 day) morphine treatment resulted in a 45% decrease in the NIL content of beta-EI and a clear depression in its basal plasma levels, although a substantial post-stress rise in plasma beta-EI was still found: stress-induced analgesia (SIA) was enhanced, but the concurrent stress-induced hyperthermia (SIH), reduced in morphinized animals. These data demonstrate that stress produces a generalized mobilization of both central and pituitary pools of beta-EI, and indicate that endorphins may play a more important role in the mediation of changes in Tc than in the generation of the concomitant increase in nociceptive threshold, upon activation by stress.

Animals↗
PubMed1984

Effects of beta-endorphin fragment 6-31 on morphine- and beta-endorphin-induced growth hormone and prolactin release.

A fragment of human beta-endorphin (beta h-EP-(6-31] has been proposed as an endogenous inhibitor of beta-endorphin. We have evaluated the effects of the fragment on beta-endorphin- and morphine-induced prolactin and growth hormone release. It inhibited both morphine- and beta-endorphin-induced prolactin release, while it was ineffective on the release of growth hormone.

Animals↗