Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of the 24-26 paraldehyde fuchsin-positive median neurosecretory cells (MNC) in the pars intercerebralis of the brain of the blowfly, Calliphora vomitoria, has shown immunoreactivity towards three different antibodies to alpha-endorphin, a peptide that corresponds to the amino acid sequence present between residues 61 and 76 of the precursor molecule, beta-lipotropin (beta-LPH). The immunoreactive material could be followed in axons within the median bundle, the tract through which neurosecretory material from the MNC is passed down to the corpus cardiacum (CC). The alpha-endorphin-immunoreactive material was observed leaving the CC in the cardiac-recurrent nerve, dorsal to the proventriculus, in the direction of the abdomen. The cells that contain the alpha-endorphin-like material are different from those of the MNC that contain insulin-, pancreatic polypeptide-, and gastrin/CCK-like peptides. This finding demonstrates the considerable complexity and peptidergic nature of the MNC and constitutes further evidence that morphinomimetic-like peptides are present in the nervous system of invertebrates.
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PMID:Immunocytochemical identification of alpha-endorphin-like material in neurones of the brain and corpus cardiacum of the blowfly, Calliphora vomitoria (Diptera). 613 86

Opioid analgesics influence the function of a number of neurotransmitter systems including classical neurotransmitters, neuropeptides and endogenous opioids. The role of these interactions in analgesia, tolerance and dependence is reviewed. Opioids inhibit the release of substance P from high threshold primary afferents, depress the activity of dorsal horn neurons and increase activity in serotonergic and noradrenergic neurons projecting from brainstem to spinal regions. Chronic administration of opioids modifies the dynamics of classical transmitters and those of endogenous opioid peptides in the brain, spinal cord and the pituitary gland. However, the effects observed are very variable. Several neuropeptides (vasopressin, MIF, alpha-MSH, CCK and dynorphin) have been reported to modify acute and chronic effects of opioids. Tolerance and dependence seen after opiate administration may involve changes in the function of these peptides.
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PMID:Opioid-neurotransmitter interactions: significance in analgesia, tolerance and dependence. 615 40

The effects of beta-endorphin, vasoactive intestinal polypeptide (VIP) and cholecystokinin octapeptide (CCK-8) on carotid chemoreceptor activity have been investigated in cats anaesthetized with pentobarbitone. Spontaneous chemoreceptor discharge was decreased by intracarotid injection of beta-endorphin and by low doses of VIP, whereas it was increased by CCK-8 and higher doses of VIP, these effects being relatively long-lasting and often associated with changes in systemic blood pressure. The chemoexcitation evoked by acetylcholine and sodium cyanide was reduced during intracarotid infusion of any of the three peptides studied, and that caused by CO2-saturated Locke solution was reduced by beta-endorphin, largely unaltered by VIP and variably affected by CCK-8. The inhibitory effect of beta-endorphin was greatly reduced by naloxone, implying that it probably involved actions at naloxone-sensitive opiate receptors in the carotid body. Substance P was unable to overcome the chemoinhibitory effect of methionine enkephalin. Possible functions of polypeptides in the carotid body are discussed.
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PMID:Effects of beta-endorphin, vasoactive intestinal polypeptide and cholecystokinin octapeptide on cat carotid chemoreceptor activity. 616 57

The present report concerns the immunocytochemistry of various peptide hormones and in particular their location in nervous structures. However, since the hormones observed in the neuroadenohypophysis and the digestive tractus have been examined elsewhere, they have been excluded from this study, except when considered outside there precise areas. The immunocytology of the following neuropeptides is presented, especially the particular details related to their demonstration: 1) The hypothalamic hypophysiotropic factor: LH-RF, SRIF, TSH-RF; derivatives from the so-called proopiocortine found by Mains and Eipper (1977), namely beta-LPH, enkephalins, endorphins, alpha-MSH- and ACTH-like antigens; 2) Prolactin and somathormone found outside the pituitary; 3) Gastro-intestinal hormones and their location outside the digestive hormones and their location outside the digestive mucosa, namely VIP, CCK, substance P; 4) Angiotensin II in nervous structures; 5) Neurotensin; 6) Thyrocalcitonin; 7) Relaxin, and the problem of its presence in the adult male genital tract. New data in invertebrate located vertebrate neuropeptides-like antigens in the nervous structures of pro-chordates (Ascidians) insects, crustaceans, annelids. These last findings underline the extensive significance of such hormonal molecules previously considered to be specific for vertebrates.
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PMID:Immunocytochemistry of polypeptide hormones: a review. 616 60

Binding of 3H-enkephalinamide and 3H-naloxone to P2-fractions of whole rat brain homogenate displayed saturable, stereospecific binding to receptor sites with at least two binding sites for 3H-metenkephalinamide (type I: KD = 0.4 nM and Bmax = 35 fmol/mg protein; type II: KD = 5.7 nM and Bmax = 57 fmol/mg protein) and for 3H-naloxone (type I: KD = 1.5 nM and Bmax = 40 fmol/mg protein; type II: KD = 51 nM and Bmax = 255 fmol/mg protein). beta-endorphin and met- and leu-enkephalin produced a concentration-dependent inhibition of 3H-met-enkephalinamide and 3H-naloxone binding with dissociation constants in the nanomolar range, but with very different displacement curves. Purified porcine ACTH (1-39) displaced both 3H-met-enkephalinamide and 3H-naloxone with dissociation constants of 3.4 X 10(-7) M and 1.8 X 10(-6) M, respectively. The synthetic congeners, ACTH (1-32) and to a lesser extent ACTH (1-28) and ACTH (1-24) showed a similar effect, whereas other fragments of ACTH were inactive in concentrations ranging from 10(10) to 10(-6) M. In the same concentration range cholecystokinin congeners (CCK-8 and CCK-4) were without effect. Since ACTH immunoreactive nerves seem also to contain beta-endorphin and furthermore, to show a partially overlapping distribution with the enkephalinergic systems it is possible that the binding of ACTH fragments to opiate receptors is of physiological relevance.
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PMID:Interaction of putative opioid peptides with opiate receptors. 626 26

We have examined the distributions of ACTH, CCK and enkephalin immunoreactive nerves in the rat central nervous system and compared the pattern obtained with that of opiate receptors. In addition, a radioreceptor assay has been employed for studying the possible functional interactions between these peptides and opiate receptors. Our results suggest that: (a) The distribution of enkephalin, CCK and ACTH/beta-endorphin immunoreactive nerve terminals is sufficiently similar to suggest functional interaction between these neuropeptides. (b) The CCK immunoreactive nerves display a distribution similar to that of enkephalin, but the main endogenous CCK forms do not bind to opiate receptors. However, opioid peptides and CCK may interact in many brain regions via binding to different, but functionally interacting receptors. (c) The ACTH immunoreactive nerves, which seem also to contain beta-endorphin, shows a partially overlapping distribution with the enkephalinergic systems. Further, ACTH and its fragments bind to opiate receptors. This suggests that ACTH could be an endogenous opioid ligand.
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PMID:Localization and opiate receptor binding of enkephalin, CCK and ACTH/beta-endorphin in the rat central nervous system. 626 60

The effects of the C-terminal octapeptide of cholecystokinin (CCK-8) and its related peptides on the onset and duration of beta-endorphin-induced catalepsy on injection of the peptides into the lateral ventricle were investigated in male rats. The onset of catalepsy was delayed to some extent by nonsulfated CCK-8 and CCK-7 but CCK-8 and caerulein were ineffective. Naltrexone and caerulein significantly shortened the duration of catalepsy, but CCKs were less effective to shorten it. Pentagastrin had no effect on either parameter.
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PMID:Suppressive effect of cholecystokinin and its related peptides on beta-endorphin-induced catalepsy in rats. 627 61

We report a detailed comparative immunocytochemical mapping of enkephalin, CCK and ACTH/beta-endorphin immunoreactive nerves in the central nervous system of rat and guinea pig. Enkephalin immunoreactivity was detected in many groups of nerve cell bodies, fibers and terminals in the limbic system, basal ganglia, hypothalamus, thalamus, brain stem and spinal cord. beta-endorphin and ACTH immunoreactivity was limited to a single group of nerve cell bodies in and around the arcuate nucleus and in fibers and terminals in the midline areas of the hypothalamus, thalamus and mesencephalic periaqueductal gray with lateral extensions to the amygdaloid area. Cholecystokinin immunoreactive nerve fibers and terminals displayed a distribution similar to that of enkephalin in many regions; but striking differences were also found. An immunocytochemical doublestaining technique, which allowed simultaneous detection of two different peptides in the same tissue section, showed that enkephalin-, CCK- and ACTH/beta-endorphin-immunoreactive nerves although closely intermingled in many brain areas, occurred separately. The distributions of nerve terminals containing these neuropeptides showed striking overlaps and also paralleled the distribution of opiate receptors. This may suggest that enkephalin, CCK, ACTH and beta-endorphin may interact with each other and with opiate receptors.
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PMID:Comparative immunocytochemical localization of putative opioid ligands in the central nervous system. 627 30

The analgesic action of beta-endorphin, as observed in the hot plate test with rats, was effectively suppressed by intracerebroventricular (i.c.v.) injection of caerulein and cholecystokinin octapeptide (CCK-8). The effect of caerulein was particularly striking; this peptide in doses of more than 0.09 nM lessened or abolished the analgesic effect of beta-endorphin in a dose of 0.7 nM. On the other hand, non sulfated CCK-8 had no significant effect on beta-endorphin-induced analgesia.
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PMID:Caerulein and cholecystokinin suppress beta-endorphin-induced analgesia in the rat. 628 27

Effects of intracerebroventricular administration of beta-endorphin, thyrotropin-releasing hormone (TRH), cholecystokinin octapeptide (CCK-8), non-sulfated CCK-8 (CCK-8-NS) and caerulein on body shaking behavior were observed in rats. CCK-8 and its related peptides produced only a small increase in the number of body shakes, while TRH had the striking effect of stimulating body shakes, this increase being markedly suppressed by simultaneous administration of beta-endorphin. Moreover, the suppressive effect of beta-endorphin on TRH-induced body shakes was antagonized by simultaneous administration of caerulein and CCK-8. The body shakes induced by ice-water immersion were also reduced by beta-endorphin, this beta-endorphin effect being partly antagonized by caerulein and CCK-8.
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PMID:Effects of beta-endorphin, thyrotropin-releasing hormone and cholecystokinin on body shaking behavior in rats. 629 91


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