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At least 73 records · Page 4Linked to original sources
PubMed1982

Non-opiate beta-endorphin fragments and dopamine--I. The neuroleptic-like gamma-endorphin fragments interfere with the behavioural effects elicited by small doses of apomorphine.

In rats, the beta-endorphin fragment, 6-17 (des-enkephalin-gamma-endorphin, DE gamma E), dose-dependently antagonized the reduction of the rate of locomotion and rearing induced by small doses of apomorphine. Structure-activity studies revealed that the active moiety of gamma-endorphin fragments with respect to counteracting apomorphine-induced behavioural changes resides in the fragment 6-17. The influence of DE gamma E appeared to be specific for dopamine systems mediating apomorphine-induced hypomotility, since DE gamma E hardly affected apomorphine-induced stereotypy and amphetamine-induced behavioural changes. These data suggest that DE gamma E acts as a dopamine antagonist selectively, on those dopamine receptor systems which are stimulated by small doses of apomorphine and which may be located presynaptically. In contrast to acute treatment, administration of DE gamma E for 4 days resulted in an enhancement of apomorphine-induced hypomotility. Thus, the receptor systems involved in these effects of apomorphine may become supersensitive upon (sub)chronic treatment with DE gamma E. The significance of the present findings are discussed in relation to the neuroleptic-like and antipsychotic action of gamma-type endorphins.

Animals↗
PubMed1982

Differences in central effects of beta-endorphin and enkephalins: beta-endorphin. A potent psychomotor stimulant.

The endogenous opiate-like peptides, beta-endorphin, methionine- and leucine-enkephalin have been investigated in unanaesthetized cats after intracerebroventricular injection. beta-Endorphin produced marked and prolonged psychomotor stimulation (restlessness, apprehension, looking around, vacant stare and impelling locomotion), accompanied by pupillary dilation and tremor which was prevented by nalorphine. In contrast to beta-endorphin, the enkephalins did not cause affective behavioural phenomena. However, the enkephalins evoked transient and inconsistent vomiting which was also prevented by nalorphine. It is apparent, therefore, that morphinomimetic brain peptides are involved in at least two functions in the central nervous system: beta-endorphin subserves the mediation of a long-lasting psychomotor stimulation, while the enkephalins mediate vomiting of a transient character.

Akathisia, Drug-Induced↗
PubMed1986

Spinal manipulation and beta-endorphin: a controlled study of the effect of a spinal manipulation on plasma beta-endorphin levels in normal males.

The role of spinal manipulation in the relief of pain is becoming clearer and more demonstrable as time passes. One approach to this study is the effect of manipulation on the neurochemical mechanisms of antinociception. Chief among these is beta-endorphin, which has been found to produce a wide range of beneficial effects, especially analgesia. The intent of our study was to demonstrate the effect of spinal manipulation on plasma beta-endorphin levels. Three groups of male subjects were randomly created: the experimental, sham and control groups. All three groups were screened for symptomatology, present use of medications and the present use of innocuous stimulants, such as nicotine and caffeine. A standard protocol involving a 20-min pretest resting period, an intervention and a 40-min test period ensued. The experimental group received a manipulation in the region of the cervical spine; the placebo group received a sham maneuver with no dynamic thrust; the control group received no intervention. Samples were taken by venipuncture at -20, -5, +5, +10 and +30 min. The data were analyzed by repeated measures analysis of variance and by Scheffe's post-hoc multiple comparison tests. Plasma beta-endorphin levels were assessed by radioimmune assay technique (according to the method described by Harber and Sutton in 1984). The results of our study demonstrated a small, but statistically significant, increase in serum beta-endorphin levels in the experimental group at the 5-min postintervention point. The levels in the placebo and control groups demonstrated a steady decrease that was distinct from the response in the experimental group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Controlled secretion of beta-endorphin from human embryonic kidney cells carrying a Tet-on-beta-endorphin fusion gene.

To create a cell line with controlled and specific secretion of beta-endorphin, a new fusion gene was constructed by joining human beta-endorphin coding sequence to part of NL1 gene. HEK293 cells carrying Tet-on system transfected with this fusion gene secreted beta-endorphin in a dose-dependent manner upon doxycycline administration. These findings suggest that this system can direct the controlled secretion of any peptide hormones such as beta-endorphin.

Cell Line↗
PubMed1982

Beta-endorphin: opiate receptor binding activities of six naturally occurring beta-endorphin homologs studied by using tritiated human hormone and naloxone as primary ligands--effects of sodium ion.

Six naturally occurring homologs of beta-endorphin were tested for their potency in inhibiting the binding of [3H]naloxone and [3H]-beta h-endorphin either in the presence or in the absence of Na+. Sodium ion reduces inhibitory potency of these homologs against [3H]-beta h-endorphin and [3H]naloxone to about the same extent. The ratio of the IC50 obtained with Na+ to that obtained without Na+ is not highly correlated with analgesic potency. Very high (greater than 300) sodium ratios are observed with some homologs. A significant rank correlation was found between the ratio of the relative potency in displacing [3H]beta h-endorphin to the relative potency in analgesia and potency in inhibiting the binding of the pure antagonist naloxone.

Animals↗
PubMed1978

Presence of immunoreactive beta-endorphin in normal human plasma: a concomitant release of beta-endorphin with adrenocorticotropin after metyrapone administration.

To elucidate whether or not beta-endorphin exists in plasma of normal subjects, plasma extracts obtained before and after metyrapone administration were subjected to gel exclusion chromatography, and fractions obtained were assayed by a sensitive radioimmunoassay for beta-endorphin. The basal plasma level of beta-endorphin was 5.8 +/- 1.1 pg/ml (mean +/- SE, n = 5), which rose significantly to the level of 48.9 +/- 3.8 pg/ml after a single oral dose (30 mg/kg of body wt) of metyrapone administration (P less than 0.001). Plasma ACTH levels also increased from the mean basal level of 73 +/- 4 pg/ml to 269 +/- 41 pg/ml after metyrapone administration. These results indicate that beta-endorphin, distinct from beta-lipotropin, exists in normal human plasma and that it is released from the pituitary concomitantly with ACTH.

Adrenocorticotropic Hormone↗
PubMed1979

ACTH, beta-LPH and beta-endorphin in pituitary adenomas of the patients with Cushing's disease: activation of beta-LPH conversion to beta-endorphin.

ACTH, beta-lipotropin (beta-LPH) and beta-endorphin concentrations were determined in pituitary adenomas of the patients with Cushing's disease. Immunoreactive ACTH and beta-endorphin were present in high concentrations and essentially equimolar amounts in pituitary adenomas. beta-LPH conversion to beta-endorphin was activated in pituitaries associated with ACTH/beta-LPH producing adenomas. Immunoreactive ACTH and beta-endorphin concentrations were markedly suppressed in the surrounding tissues.

Adenoma↗
PubMed1976

[Endorphins, hypothalamic and neurohypophysial peptides with morphinomimetic activity: isolation and molecular structure of alpha-endorphin].

From a crude extract of Porcine neurohypophysis-hypothalamus we have isolated several peptides called endorphins which mimic opiated in a classical bioassay for morphine. Similarly they bind to the stereospecific synaptosomal opiates receptors of Rat brain in competition to 3 H-etorphine. The primary structure of alpha-endorphin is H-Tyr-Gly-Gly-Phe-Met-Thr-Ser-Glu-Lys-Ser-Gln-Thr-Pro-Leu-Val-Thr-OH. Met-enkephalin is the N-terminal pentapeptide of alpha-endorphin. Alpha-endorphin has the same sequence as that of the fragment TYR 61 to Thr 76 of the beta-lipotropins.

Amino Acid Sequence↗
PubMed1984

Effect of various behavioral training and testing procedures on brain beta-endorphin-like immunoreactivity and the possible role of beta-endorphin in behavioral regulation.

Beta-Endorphin-like immunoreactivity is reduced in the rat diencephalon after the animals are exposed for the first time to any of the following behavioral situations: 50 tones (habituation), 50 tone-footshock shuttle avoidance trials, one step-down inhibitory avoidance trial, simple exposure to the avoidance apparatus with no footshocks, or inescapable shock. The effect is not observed when animals are exposed to any of these situations for a second time. The reduction of brain beta-endorphin-like immunoreactivity is attributable to release and subsequent metabolism of the substance, and correlates with the novelty inherent in the diverse training or test situations. The role of beta-endorphin in behavior is discussed in the light of these and previous results which showed that it causes both retrograde amnesia and a facilitation of retrieval. The substance would appear to serve an adaptive function when animals are exposed to a new experience, by inducing a temporary forgetting of the experience together with (or leading to) a state of alertness or preparedness for what may happen next.

Acoustic Stimulation↗
PubMed1985

The course of the decrease of hypothalamic beta-endorphin induced by training, and the development of the effect of beta-endorphin on the retrieval of inhibitory avoidance in rats.

Step-down inhibitory avoidance training or the simple exposure of rats to the training apparatus is followed by a decrease of hypothalamic beta-endorphin immunoreactivity at 0.1, 1.0 or 2.0 h after training. Immunoreactivity returns to normal at 6.0 h. The ip administration of 1.0 microgram/kg of human beta-endorphin 6 min prior to training produces an inhibition of the retrieval of the step-down task at 6.0 h, but not at 0, 1.0 or 2.0 h after training. This effect is reversed by a second injection of the substance immediately before testing. The possible physiological significance of this parallel development of the effect of beta-endorphin on retrieval and the depletion of the substance caused by training is discussed. The data indicate that retrieval is insensitive to the peptide when its hypothalamic stores are depleted.

Animals↗
PubMed1979

Systemic administration of Met-enkephalin, (D-Ala2)-Met-enkephalin, beta-endorphin, and (D-Ala2)-beta-endorphin: effects on eating, drinking and activity measures in rats.

Rats were given four daily, interperitoneal injections (80 micrograms/kg) of Met-enkephalin, (D-Ala2)-Met-enkephalin-NH2, beta-endorphin, (D-Ala2)-beta-endorphin or the diluent (0.9% NaCl acidified to, 0.01 M with acetic acid). Animals were subsequently tested for food and water inake and activity. Met-enkephalin injections did not affect any of the measures but its (D-Ala2) analog reduced food intake and some of the activity measures in a complicated way. beta-Endorphin injections did not affect food or water intake; in familiar situations these animals were less active while novel situations seemed to potentiate activity. The (D-Ala2) analog reduced wheel running over 24 hours.

Animals↗
PubMed1985

Introduction to symposium on endorphins and behavioural processes; review of literature on endorphins and exercise.

The first symposium on endorphins and behavioural processes in Britain was held by the British Psychological Society in March 1985. Against a background of the explosive history of the discovery of endogenous opioids, problems of terminology, and basic mechanisms and concepts, five papers reflect the main fields in which outstanding progress has been made: analgesia, feeding, reward mechanisms, social behaviour and aggression, and addiction. A review of the literature on endorphins and exercise stresses both the value and limitations of trying to unravel a fashionable subject. Endorphin research is multi-disciplinary and highly complex, with tricky technical and conceptual problems and inevitable lack of consensus. Investigators should be more aware of the crucial role that outcomes of behaviour experiments play in the attribution of function to opioid systems.

Analgesia↗
PubMed1992

Central changes of beta-endorphin-like immunoreactivity during rat tonic pain differ from those of purified beta-endorphin.

Several studies have described changes in beta-endorphin-like immunoreactivity (beta-ELI) in the rat brain in response to pain and stress stimuli. In order to ascertain the components of beta-ELI, brain samples of rats experiencing acute prolonged (tonic) pain were evaluated for their beta-ELI and later submitted to a chromatographic purification allowing the measurement of beta-endorphin (beta-EP) and acetyl beta-EP. The chromatographic analysis of both ventromedial hypothalamus (VMH) and periaqueductal grey (PAG) homogenates indicates that beta-ELI is distributed in several fractions including shortened forms of beta-EP and their respective acetylated compounds. Quantitatively, while beta-ELI in formalin-injected animals was increased by 48% in VMH and 45% in PAG in respect to controls, the net increase of purified beta-EP was 1100% and 470%, respectively, for VMH and PAG. Moreover, the maximal increase of beta-ELI was evident at 120 min, in both tissues. In contrast, the beta-EP peak was reached at 30 min in VMH and at 60 min in PAG. Acetyl beta-EP was unchanged by treatment in both central areas. No correlation of beta-ELI and beta-EP was found in VMH. These data demonstrate that the evaluation of beta-ELI gives a poor estimate of beta-EP changes, due to several components of the endorphin family.

Animals↗
PubMed2003

Beta-endorphin-like peptide SLTCLVKGFY reduces the production of 11-oxycorticosteroids by rat adrenal cortex through nonopioid beta-endorphin receptors.

Beta-endorphin-like peptide immunorphin (SLTCLVKGFY), a selective agonist of nonopioid beta-endorphin receptor, was labeled with tritium to specific activity of 24 Ci/mmol. It was used for the detection and characterization of nonopioid beta-endorphin receptors on rat adrenal cortex membranes (Kd = 31.6 +/- 0.2 nM, Bmax = 37.4 +/- 2.2 pmol/mg protein). Immunorphin at concentrations of 10(-9) to 10(-6) M was found to inhibit the adenylate cyclase activity in adrenal cortex membranes, while intramuscular injection of immunorphin at doses of 10-100 microg/kg was found to reduce the secretion of 11-oxycorticosteroids from the adrenals to the bloodstream.

Adenylyl Cyclase Inhibitors↗
PubMed2003

The Stimulating Effect of the beta-Endorphin-Like Peptide Immunorphin on the Human T-Lymphoblastoid Cell Line Jurkat Is Mediated by a Non-Opioid Receptor for beta-Endorphin.

It was shown that beta-endorphin and the synthetic decapeptide SLTCLVKGFY that corresponds to the amino acid sequence 364-373 of the human IgG heavy chain (referred to as immunorphin) is able to stimulate growth of the human T-lymphoblastoid cell line Jurkat. The antagonist of opioid receptors naloxone did not inhibit the stimulating effect of the peptides. Studies on [(3)H]-immunorphin binding to Jurkat cell receptors have demonstrated that it binds with high affinity to naloxone-insensitive receptors (K(d) = 1.3 nM; n = 5.2 x 10(5)). Unlabeled beta-endorphin and the 6-10 fragment of immunorphin completely inhibited the labeled ligand specific binding to naloxone-insensitive receptors on T lymphocytes (K(i) = 1.4 x 10(-7) and 3.7 x 10(-5) M, respectively). Thus, beta-endorphin and immunorphin share the naloxone-insensitive receptors on human T-lymphoblastoid cell line Jurkat.

Humans↗
PubMed1989

Immunoregulatory effects of alpha-endorphin, beta-endorphin, methionine-enkephalin, and adrenocorticotropic hormone on anti-tetanus toxoid antibody synthesis by human lymphocytes.

This study assesses the effects of adrenocorticotropic hormone (ACTH), alpha-endorphin (alpha-endo), beta-endorphin (beta-endo), and methionine-enkephalin (met-enk) on tetanus toxoid-stimulated in vitro specific antibody (anti-TT) synthesis. ACTH and TT-costimulated cultures enhanced antibody (Ab) synthesis over control TT-stimulated cultures at 10(-9) and 10(-11) M and suppressed Ab synthesis at 10(-13) and 10(-17) M. The alpha-endo and TT-costimulated cultures enhanced Ab synthesis over control cultures at all concentrations tested (10(-7) to 10(-15) M). Cultures costimulated with beta-endo and TT enhanced Ab synthesis over control cultures at 10(-11) M and suppressed Ab synthesis at doses above and below 10(-11) M. The met-enk and TT-costimulated cultures produced more Ab than controls at 10(-9) M; and the met-enk and TT-costimulated cultures produced less Ab than controls at other concentrations as low as 10(-17) M and as high as 10(-7) M. The results of this study provide one reason as to why the interactions between the neuroendocrine and immune systems remain unclear.

Adrenocorticotropic Hormone↗
PubMed1983

Localization and identification of gamma-endorphin and beta-endorphin-like peptides in the hypothalamus and ventral forebrain of the rat.

Gamma-endorphin (gamma E) and related peptides were localized in the brain of the rat, and compared to the distribution of beta-endorphin related peptides. gamma E-like immunoreactivity (gamma E-LI) was shown to exist only in brain regions known to receive innervation from POMC neurons but not in their pericaria in the arcuate nucleus. Nuclei of the hypothalamus and ventral forebrain contained the major concentration of gamma E-LI and extracts from these regions were purified and subjected to HPLC in order to identify gamma E-related peptides. gamma E, des-tyrosine1 gamma E, des-enkephalin-gamma E, and alpha-N acetyl gamma E co-elutable peptides as well as various unidentified forms were evident. This study provides evidence of the endogenous presence of pharmacologically active gamma E-related peptides in brain regions where they have been postulated to modulate dopaminergic transmission.

Animals↗
PubMed1990

[Structural organization of [met]enkephalin and endorphin molecules. II. Theoretical conformation analysis of alpha-, gamma- and delta-endorphins].

Conformational energy calculations were carried out for neuropeptides alpha-, gamma- and delta-endorphins, which are 1-16, 1-17 and 1-19 fragments respectively, of beta-endorphin. The proposed computational scheme yielded all possible low-energy conformational sets for these hormones. Specific features of spatial organization of each compound and similarities of their structures are discussed.

Amino Acid Sequence↗