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)

The immune system and the neuroendocrine system affect each other via molecules and receptors shared by both systems. Neuroendocrine hormones may act either positively or negatively in regulating the activities of a key cell of the immune system, the macrophage. For example, adenocorticotropic hormone (ACTH), somatostatin, and substance P are all capable of increasing the cytotoxicity of macrophages against tumor cells. However, ACTH and somatostatin, but not substance P, can also block the tumoricidal activity of macrophages induced by recombinant gamma interferon (IFN-gamma), a non-neuroendocrine immunomodulating hormone. In contrast, substance P increased tumoricidal activity, both independent of IFN-gamma and in addition to IFN-gamma. Neurotensin, alpha-endorphin, beta-endorphin, met-enkephalin, vasopressin, and substance K did not affect tumoricidal function, either alone or in combination with IFN-gamma. Substance P, but not the other neuropeptides, increased substantially the proportion of macrophages able to secrete superoxide ions, suggesting a possible influence on macrophage capacity to deal with microbial infection. Such positive and negative modulation of macrophage effector functions could contribute to the influence of cognitive stimuli in infection and neoplasia.
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PMID:Neuropeptides modulating macrophage function. 303 73

Neurotensin (NT), administered intracisternally to mice, produced significant dose-dependent antinociception in three analgesic tests: tail immersion, hot-plate and acetic acid writhing. Naloxone (1-5 mg/kg), an opiate antagonist administered i.p. 20 min before NT administration, did not significantly alter NT-induced antinociception in any of these tests; naloxone did significantly reverse beta-endorphin-induced antinociception. However, centrally and peripherally administered thyrotropin-releasing hormone antagonized NT-induced (but not beta-endorphin-induced) antinociception. Equimolar doses of another tripeptide (Pro-Leu-Gly-NH2; melanostatin) did not alter the effects of NT. The data obtained in this study confirm NT-induced antinociception, provide further evidence that NT does not activate naloxone-sensitive opiate receptors and demonstrate that this brain effect of NT is antagonized by thyrotropin-releasing hormone. These findings therefore support the hypothesis that NT and thyrotropin-releasing hormone are functional antagonists in the central nervous system.
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PMID:Neurotensin-induced antinociception in mice: antagonism by thyrotropin-releasing hormone. 611 61

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

The effects of intracerebroventricular administration of several peptides on discrete-trial, conditioned avoidance responding were assessed in the rat. Three peptides (neurotensin, bombesin and beta-endorphin) produced a neuroleptic-like effect (i.e. a decrease in avoidance responding with no effect on escape responding). A low dose (0.6 nmol) of each peptide elicited a significant effect. Neurotensin and bombesin produced a significant but partial decrease in avoidance responding; larger doses of these peptides did not produce a greater effect. beta-Endorphin elicited dose-related decrements in avoidance responding. In addition, the effect of neurotensin, but not bombesin or beta-endorphin, was antagonized by simultaneous administration of an equimolar dose of thyrotropin-releasing hormone. Hence, the 3 peptides do not appear to produce decreases in avoidance responding by the same mechanism. Thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, bradykinin, substance P, des-Tyr1-gamma-endorphin and melanotropin inhibiting factor did not significantly affect avoidance responding. These findings, taken together with previous findings, suggest that intracerebroventricular administration of certain endogenous peptides (neurotensin, bombesin and beta-endorphin) may exert neuroleptic-like effects.
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PMID:The effects of neuropeptides on discrete-trial conditioned avoidance responding. 617 91

Neurotensin (NT) and bombesin, which are heterogeneously distributed in both brain and gastrointestinal tissue of several mammalian species, inhibit the formation of stress-induced gastric ulcers in rats. Many other endogeneous neuropeptides have also been reported to be present in brain and gastrointestinal tissue. The present study was conducted to evaluate the effect of some of these peptides on the development of cold-restraint stress (CRS)-induced gastric ulcers in rats. In addition, the effect of thyrotropin-releasing hormone (TRH), which antagonizes many of the CNS effects of NT, was investigated to determine whether this tripeptide antagonizes the cytoprotective effect of NT in this CRS model. All peptides were initially administered intracisternally (ic) in doses equimolar to 30 micrograms NT. As previously reported, NT (30 micrograms, ic) completely prevented the development of gastric ulcers in rats exposed to three hours of CRS. Bombesin, beta-endorphin, substance P, and somatostatin also exhibited cytoprotective activity. Several other peptides studied in the CRS model exerted no significant effects on the development of gastric ulcers; these included cholecystokinin octapeptide, gastrin, leu-enkephalin, met-enkephalin, and bradykinin. Two peptides, vasoactive intestinal polypeptide and TRH, significantly increased the severity of gastric ulcerations. The cytoprotective effect of NT was dose dependent. In contrast, lower doses of beta-endorphin, substance P, and somatostatin were cytoprotective whereas higher doses were not. Finally, concomitant ic injections of TRH antagonized the cytoprotective effects of NT and bombesin, but not that of beta-endorphin. The present results suggest that certain brain peptides may participate in modulating the gastric mucosal barrier, thereby increasing or decreasing its vulnerability to stress-induced lesions.
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PMID:The effect of centrally administered neuropeptides on the development of stress-induced gastric ulcers in rats. 630 95

The effects of the three peptides neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors were studied in mice. Intracisternal administration of these peptides to mice prolonged the duration of sleep induced by ethanol (5.2 g/kg). Neurotensin and beta-endorphin also enhanced ethanol-induced hypothermia. None of the peptides, when administered alone, produced sleep. However, all three compounds impaired the aerial righting reflex and induced sleep when followed by an IP dose of ethanol (3.5 g/kg), which alone did not induce sleep. These results, taken together with previous findings, suggest that neuropeptides may be involved in the complex mechanisms of action of ethanol on the CNS.
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PMID:The effects of neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors in mice. 630 2

The guinea-pig intestine was found to harbor nerve fibers containing immunoreactive cholecystokinin (CCK), gastrin-releasing peptide (GRP), neurotensin or beta-endorphin. Such fibers occurred in the myenteric and submucous ganglia and in the smooth muscle. GRP- and CCK-fibers, in addition, were found in the mucosa. Following colchicine treatment, neuronal perikarya in the myenteric ganglia displayed CCK-, GRP-, or beta-endorphin immunoreactivity. CCK-immunoreactive perikarya were located also in the submucous ganglia. Neurotensin-immunoreactive cell bodies could not be detected. The presence of immunoreactive neuronal perikarya in intramural ganglia indicates that CCK-, GRP- and beta-endorphin-containing fibers are intrinsic to the gut wall. GRP, neurotensin, and beta-endorphin were identified in extracts of smooth muscle by immuno-chemical and chromatographic analysis. CCK-8, GRP and neurotensin contracted the isolated taenia coli. Tetrodotoxin reduced the response to CCK-8 but not that to GRP and neurotensin, suggesting that the two latter peptides act directly on smooth muscle receptors. The effect of CCK-8 is partly mediated by cholinergic nerves, since not only tetrodotoxin but also atropine greatly reduced the CCK-8-induced contractile response. The substance P (SP) antagonist, (D-Pro2, D-Trp7,9)-SP1-11 had no effect on the CCK-8-induced contraction of the taenia. CCK-8 enhanced the SP-mediated (atropine-resistant) contractile response to electrical stimulation but not that mediated by acetylcholine. beta-Endorphin had no effect on the tension of the muscle but reduced the response to electrical stimulation (cholinergic as well as SP-mediated) through a naloxone-sensitive mechanism. While CCK-8 and beta-endorphin seem to play neuromodulatory roles in the taenia coli, the significance of GRP and neurotensin remains enigmatic.
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PMID:Neuronal cholecystokinin, gastrin-releasing peptide, neurotensin, and beta-endorphin in the intestine of the guinea pig. Distribution and possible motor functions. 632 15

Neurotensin (NT), an endogenous tridecapeptide, is heterogeneously distributed in the central nervous system. The present study examined the effects of physiologically and behaviorally active doses of NT (1--100 micrograms intracisternally) on dopamine, serotonin and their primary metabolites as well as accumulation of dopa after inhibition of dopa decarboxylase. NT was shown to increase dopa accumulation when compared with saline treatment, suggesting that dopamine synthesis was increased. In accord with this view, NT also caused a dose-dependent increase in homovanillic acid and dihydroxyphenylacetic acid, the major metabolites of dopamine, in several brain areas (striatum, olfactory tubercles, nucleus accumbens, frontal cortex and hypothalamus). Interestingly, the increase in homovanillic acid was greater than that for dihydroxyphenylacetic acid. In striatum, an initial increase in dopamine content after 30 micrograms of NT was followed by an increase and a subsequent decrease of dopamine metabolites. Several other neuropeptides (Met-enkephalin, cholecystokinin-8, thyrotropin releasing hormone, substance P and d-Arg9-NT), at doses equimolar to 30 micrograms of NT, did not affect dopamine metabolites, whereas certain others (beta-endorphin and bombesin) increased their concentration in some brain areas. Except for the highest dose of NT, measures of serotonergic function were not affected by NT or any of the other neuropeptides.
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PMID:Increase in dopamine metabolites in rat brain by neurotensin. 681 28

The paraventricular nucleus of the hypothalamus (PVH) is innervated by a variety of types of neuropeptide-immunoreactive fibers. The cells of origin for many of these inputs are not known. In the present study, the combined retrograde fluorescence-immunofluorescence method was used to determine the cells of origin for neurotensin-, corticotropin-releasing factor-, brain natriuretic peptide-, somatostatin-, and met-enkephalin-like immunoreactive (-ir) fibers in the PVH. After injections of the fluorescent tracer Fluorogold into the PVH, the pattern of retrograde labeling was as previously reported (Sawchenko and Swanson, 1983, J. Comp. Neurol. 218:121-144; McKellar and Loewy, 1981, Brain Res. 217:351-357). The distribution of each type of double-labeled neuron was unique. Retrogradely labeled enkephalin-ir neurons were concentrated in two locations: the ventral part of the lateral septal nucleus and the lateral anterior nucleus within the AHA. A small cluster of corticotropin-releasing factor-ir neurons in the ventral lateral subnucleus of the bed nucleus of the stria terminalis were retrogradely labeled. Notable concentrations of somatostatin-ir double-labeled neurons were found in the ventral part of the lateral hypothalamic area and the medial part of the arcuate hypothalamic nucleus. Neurotensin-ir double-labeled neurons were most numerous in the anteroventral periventricular nucleus and in the retrochiasmatic area. Many brain natiuretic peptide-ir neurons in the tuberomammillary nucleus of the hypothalamus and in the pedunculopontine and laterodorsal tegmental nuclei were retrogradely labeled. The specificity of these chemically defined projections helps lay the groundwork for examining the functional organization of PVH afferents.
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PMID:Neuropeptide-immunoreactive neurons projecting to the paraventricular hypothalamic nucleus in the rat. 796 8

These studies examined the role of the neurotensinergic projections extending from the periaqueductal gray (PAG) to the nucleus raphe magnus (NRM) on the inhibition of the tail-flick reflex produced by microinjection of morphine or beta-endorphin in the PAG. Neurotensin (3-30 nmol) or the partial agonist [D-Trp11] neurotensin (100 and 300 pmol) microinjected into the NRM of awake rats produced a dose-dependent inhibition of the tail-flick response lasting 90 to 150 min. Lower doses of neurotensin (0.03-0.3 nmol) produced a hyperreflexive tail-flick response 10 min after injection, which correlated with a decreased hot plate latency. Additionally, a dose of [D-Trp11]neurotensin (3 pmol) that had no intrinsic activity antagonized both the antinociceptive as well as hyperreflexive responses of neurotensin. Morphine (6 nmol) injected into the PAG produced an inhibition of the tail-flick response that was enhanced by injection of [D-Trp11]neurotensin (3 pmol) into the NRM. In contrast, injection of [D-Trp11]neurotensin (3 pmol) into the NRM had no effect on the inhibition of the tail-flick produced by beta-endorphin (10 nmol) in the PAG. Antineurotensin antiserum yielded results similar to those obtained with [D-Trp11]neurotensin. Although neurotensin was found to produce changes in tail skin temperature, it was possible to dissociate these effects from changes in tail-flick latency. These data suggest that neurotensin produces both antinociceptive and hyperalgesic responses when injected into the NRM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of neurotensin in the nucleus raphe magnus in opioid-induced antinociception from the periaqueductal gray. 849 8


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