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At least 19 recordsLinked to original sources
PubMed1978

Immunocytological detection and localization of a peptide reacting with an alpha-endorphin antiserum in the corticotropic and melanotropic cells of the trout pituitary (Salmo irideus Gibb).

In the pituitary of the trout, the corticotropic and melanotropic cells display a strong immunocytological reaction with alpha-endorphin antiserum. This reaction persists even when alpha-endorphin antisera treated with beta-1-24ACTH or alpha-MSH are used. In the absence of pharmacological tests on the endorphic potencies of the compounds involved in the immunoreaction, it is not yeat clear whether this reaction is due to the presence of an alpha-endorphin-like peptide or simply an immunologically related peptide without the properties of endorphin. However, the presence of such peptides in the fish pituitary is interesting from the comparative point of view.

Adrenocorticotropic Hormone↗
PubMed1977

[Immunocytological localization of peptide analogs of alpha-endorphin in several neurons of the lateral nucleus tuberis of Carassius auratus L. and Cyprinus carpio L].

Neurons of the pars lateralis of the N.L.T. of Carassius auratus and Cyprinus carpio display a positive immunocytological reaction with an anti alpha-endorphin serum. It is assumed that the peptides produced by these neurons are similar, if not identical, with alpha-endorphin, but their morphinomimetic properties have still to be established. Peptides of this kind may participate in the regulation of pituitary functions.

Animals↗
PubMed1979

[Localization of immunoreactive sites with anti met-enkephalin and anti alpha-endorphin sera in carp brain].

In the brain of the Carp an anti met-enkephalin serum reveals some telencephalic fibres, about half of the N.P.O. cells and furthermore a subependymal zone of nervous tissue close to the third ventricle of the superior hypothalamus and thalamus. These structures do not react with an anti alpha-endorphin serum, which however reveals cells of the lateral N.L.T. and the corresponding fibres.

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↗
PubMed1978

[Immunocytology of alpha-endorphin positive hypothalamic fibers of Carassius auratus L. and Cyprinus carpio L].

An immunocytological study of the basal hypothalamus of Carassius auratus and Cyprinus carpio with an alpha-endorphin antiserum shows the different nerve processes belonging probably to the immunoreactive cells of the lateral part of the N.L.T. According to their pathways, two main fibre tracts have been distinguished: many fluorescent fibres converge towards the pituitary gland into which they enter, other fibres run caudally through the tuber towards the nucleus tuberis inferior (Baumgarten and Braak) where they could not be followed further.

Animals↗
PubMed1978

Behavioral and electrophysiological effects of peptides related to lipotropin (beta-LPH).

Both C-terminal fragments of lipotropin (beta-LPH) (endorphins) and N-terminal fragments (e.g., ACTH 4-10) delayed extinction of pole-jumping avoidance behavior in rats. After subcutaneous injection Met5-enkephalin appeared to be as active as ACTH 4-10 whereas beta-LPH 61-69, alpha- and beta-endorphin were more potent in delaying extinction of pole-jumping avoidance behavior (approximate ED50 of alpha-endorphin 4 x 10(-11) M rat.) However, the potency of beta-LPH 61-69 and alpha-endorphin appeared to be approximately the same whereas that of beta-endorphin was less than that of ACTH 4-10 after intraventricular administration (approximate ED50 of alpha-endorphin 0.2 x 10(-11) M rat). alpha-Endorphin and ACTH 4-10, administered subcutaneously in a dose which markedly delayed extinction of pole-jumping avoidance behavior, had only slight effects on open field behavior and on responsiveness to electric footshock. A 5 times higher dose of both peptides facilitated passive avoidance behavior. Morphine in two doses significantly delayed extinction of pole-jumping avoidance behavior but the effect was not dose dependent. The specific opiate antagonist naltrexone, however, markedly facilitated extinction of the avoidance response. ACTH 4-10, alpha- and beta-endorphin and a behaviorally potent ACTH 4-9 analog (Org 2766) restored pole-jumping avoidance behavior of rats pretreated with naltrexone. Treatment with a similar dose of naltrexone blocked beta-endorphin-induced analgesia. These results suggest that the influence of peptides related to C-terminal and N-terminal fragments of lipotropin on extinction of avoidance behavior may be dissociated from those exerted on opiate receptor sites. Subcutaneously injected beta-LPH 61-69 or intraventricularly administered beta-endorphin induced a shift from lower to higher frequencies of hippocampal theta rhythm during paradoxical sleep in the same way as that found after ACTH 4-10. This effect is interpreted as indicating an increased arousal state in certain midbrain limbic structures. This may, as has been postulated for ACTH 4-10, alter the motivational value of environmental stimuli (e.g., aversive stimulation).

Adrenocorticotropic Hormone↗
PubMed1978

Cardiovascular effects of morphine and opioid peptides following intracisternal administration in chloralose-anesthetized rats.

Beta-Endorphin (0.9--2.0 nmol), morphine (11--250 nmol) and D-ala2-met-enkephalinamide (17--33 nmol) administered intracisternally produced preferential vasodepressor responses and bradycardia. Leu- (1.8--180 nmol), met-enkephalin (17--520 nmol) and alpha-endorphin (5.7--57 nmol) administered in the same way produced preferential vasopressor effects and the latter two peptides also produced bradycardia. Results obtained with naloxone (300 nmol) given intracisternally indicate that the pressor and depressor actions as well as the bradycardia are mediated through opiate receptors. The results indicate that opioid peptides may be involved in central cardiovascular control.

Anesthesia↗
PubMedDate not supplied

Reduction of distress vocalization in chicks by opiate-like peptides.

All the opiate-like peptides we tested (Met-enkephalin, (D-Ala2)-Met-enkephalin-NH2, beta-endorphin, (D-Ala2)-beta-endorphin, (D-Ala2)-alpha-endorphin, (D-Ala2)-gamma-endorphin) were capable of reducing distress vocalizations (DV's) in socially-isolated chicks when injected into the vicinity of the fourth ventricle in doses as low as 100 picomoles. All of these substances were at least as potent as equimolar doses of morphine sulfate. In general, DV's were a more sensitive measure of opiate-like peptide effects than reductions in body temperature. In a more limited study using peripheral injections, it was determined that (D-Ala2)-Met-enkephalin at doses of 400 nanomoles/kg, like morphine sulfate, was more effective in reducing DV's, than an equimolar dose of beta-endorphin. beta-endorphin was not as effective via a peripheral route as it was via central administration.

Animals↗
PubMed1977

Isolation and characterization of the opioid peptides from rat pituitary: beta-endorphin.

beta-Endorphin was isolated from 200 rat pituitaries by means of high-performance column chromatography, using sensitive fluorometric methods and a radioreceptor assay for opioid activity. The beta-endorphin was characterized as to molecular weight, amino acid composition, and mapping of tryptic peptides by a new microtechnique. It was found that rat beta-endorphin is identical to camel and sheep beta-endorphin. Furthermore, alpha-endorphin, Met-enkephalin, a nonpeptide morphine-like compound (MLC), and an additional unidentified opioid compound were detected in the extract of rat pituitary.

Amino Acids↗
PubMed1978

Neurons containing beta-endorphin in rat brain exist separately from those containing enkephalin: immunocytochemical studies.

Well-characterized antisera to porcine beta-endorphin were used to localize immunoreactive sites in cryostat sections of formaldehyde-fixed rat brain by indirect immunohistochemistry. Specificity was established by absorption of immune sera with synthetic peptide fragments. Specific immunoreactivity was localized to neuronal perikarya in the basal tuberal hypothalamus, and to varicose nerve fibers which were distributed to midline nuclear areas throughout the diencephalon and anterior pons. These patterns of reactivity were unaffected by preabsorption of the immune sera with millimolar concentrations of Met5- or Leu5-enkephalin or alpha-endorphin. The beta-endorphin immunoreactive structures were morphologically separate from those cells and fibers reported to react with antisera to the enkephalins. One anti-beta-endorphin serum gave additional immunoreactivity with myelinated axons in limbic cortical zones; when absorbed with purified rat myelin basic protein, only the specific patterns of immunoreactivity remained. Thus, discrete beta-endorphin-containing neuronal circuits exist in rat brain and are anatomically distinguishable from enkephalin-containing nerve cell and fiber pathways.

Animals↗
PubMed1977

The distribution of methionine-enkephalin and leucine-enkephalin in the brain and peripheral tissues.

1 A method is described for the rapid extraction of opioid peptides from the brain and other tissues. The method is based on acid extraction of tissues followed by adsorption of the extract onto Amberlite XAD-2 resin. Elution with methanol separates the enkephalins and alpha-endorphin from beta-endorphin.2 Over 90% of the opioid peptide activity isolated from brain and gut of several species by our method was due to methionine- and leucine-enkephalin. In contrast, the major opioid peptide activity recovered from the pituitary was due to peptides of much greater mol. wt. than the enkephalins.3 An opioid peptide with properties unlike those of the known endorphins or enkephalins was present in brain extracts. This peptide, termed epsilon-endorphin, has an apparent mol. wt. of 700 to 1200; it constituted between 5 to 10% of the total opioid activity in our extracts.4 A differential assay of methionine- and leucine-enkephalin was made either by destroying methionine-enkephalin activity with cyanogen bromide or by separating the peptides by thin layer chromatography.5 The ratio of methionine-enkephalin to leucine-enkephalin varied greatly in different brain regions. The highest proportions of leucine-enkephalin were found in the cerebral cortex and hippocampus.6 Formaldehyde perfusion and fixation of the brain in vivo had no significant effect on the brain content of enkephalin, indicating that proteolytic breakdown is not a major problem in the extraction of these peptides.7 It is suggested that the enkephalins may have a neurotransmitter role in both brain and peripheral tissues and that methionine- and leucine-enkephalin may subserve separate neuronal functions.

Animals↗
PubMed1976

The C-fragment of beta-lipotropin: an endogenous neuroleptic or antipsychotogen?

Microinjection of the C-fragment (also called beta-endorphin), which is amino acid sequence 61-91 of the endogenous pituitary hormone, beta-lipotropin (beta-LPH), in the periaqueductal gray of the rat resulted in profound sedation and catalepsy, while microinjection of smaller fragments-that is, methionine-enkephalin [sequence beta-LPH-(61-65)] and its related pentapeptide, leucine enkephalin, and alpha-endorphin [sequence beta-LPH-(61-76)] resulted in attenuated forms of this behavior. This indicates that the C-fragment is an important neuromodulator of the central nervous system. The similarity of this behavior to that seen after systemic administration to experimental animals of exogenous neuroleptics suggests that a disturbance in the bioavailability of this neuropeptide to receptor sites in brain-perhaps due to lack of enzymatic cleavage from the circulating parent hormone, beta-lipotropin--may be an etiological factor in those psychopathological states for which the exogenous neuroleptics exert an ameliorative influence.

Analgesia↗
PubMed1979

Specific nonopiate receptors for beta-endorphin.

Iodinated beta H-[2-D-alanine]endorphin exhibits specific binding to cultured human lymphocytes. The binding is inhibited by low concentrations of beta-endorphin and its D-alanine derivative, but is not affected by opiate agonists and antagonists, or by enkephalin analogs, beta-lipotropin, adrenocorticotrophic hormone, or alpha-melanocyte-stimulating hormone; this suggests the existence of a specific, non-opiate binding site (receptor) for beta-endorphin. The carboxy-terminal region of beta-endorphin is essential for this binding activity, since alpha-endorphin is not active. beta-Endorphin may be a circulating hormone with peripheral physiological effects that are not primarily mediated through interactions with opiate or enkephalin receptors.

Amino Acid Sequence↗