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)

Recently the pH gradient evoked by a K+ diffusion potential was shown to translocate a synthetic monobasic amphipathic hexapeptide across the bilayer of lipid vesicles (De Kroon, A.I.P.M., Vogt, B., Van 't Hof, R., De Kruijff, B. and De Gier, J. (1991) Biophys. J. 60, in press). Here this observation is extended by studying the effect of a membrane potential on a set of bioactive peptides. The panel of peptides comprises the toxin mastoparan X, a tryptophan-containing analogue of the presequence of the mitochondrial protein cytochrome oxidase subunit IV (preCoxIV(1-25)W18), and the regulatory peptides ACTH(1-24), alpha-MSH, ACTH(1-10), dynorphin A, bombesin, and LHRH. The interaction of these peptides with phospholipid vesicles has been measured using the intrinsic tryptophan residue as fluorescent probe. In the absence of a K+ diffusion potential only mastoparan X and the presequence show considerable binding to vesicles consisting of phosphatidylcholine (PC). In contrast, under these conditions all peptides display affinity for vesicles consisting of the acidic phospholipid cardiolipin (CL), the extent of which depends on the net positive charge of the peptide. Application of a K+ diffusion potential to large unilamellar vesicles (LUV) consisting of PC results in a time dependent tryptophan fluorescence increase for mastoparan X, which is accelerated upon incorporating increasing amounts of CL into the LUV. A similar fluorescence increase in response to a K+ diffusion potential was observed for the above model peptide. Yet the mechanism resulting in the fluorescence increase of mastoparan X is completely different from that of the hexapeptide. Binding experiments indicate that a membrane potential-induced enhanced binding of the peptide to the outer surface of the vesicles contributes to the fluorescence increase. PreCoxIV(1-25)W18, dynorphin A, and ACTH(1-24) show fluorescence responses upon applying a membrane potential that are consistent with that of mastoparan X, whereas the other peptides tested do not respond up to a LUV CL content of 50%. The results tentatively suggest that the membrane potential only affects a peptide when it has the ability to adopt a stable membrane bound conformation.
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PMID:The effect of a membrane potential on the interaction of mastoparan X, a mitochondrial presequence, and several regulatory peptides with phospholipid vesicles. 168 Mar 97

Autonomic dysfunction is an increasingly recognized problem in aging animals and man. The pathologic changes that produce autonomic dysfunction in human aging are largely unknown; however, in experimental animal models specific pathologic changes have been found in selected sympathetic ganglia. To address whether similar neuropathologic changes occur in aging humans, the authors have examined paravertebral and prevertebral sympathetic ganglia from a series of 56 adult autopsied nondiabetic patients. They found significant, specific, age-related neuropathologic lesions in the prevertebral sympathetic superior mesenteric ganglia of autopsied patients. Markedly swollen dystrophic preterminal axons compressed or displaced the perikarya of principal sympathetic neurons. Ultrastructurally, these swollen presynaptic axons contained abundant disoriented neurofilaments surrounded by peripherally marginated dense core vesicles. Immunohistochemical studies demonstrated that dystrophic axons contained tyrosine hydroxylase and neuropeptide tyrosine (NPY)-like immunoreactivity but not other neuropeptides (VIP, substance P, gastrin-releasing peptide [GRP]/bombesin, met-enkephalin). Similar to the animal models of aging, lesions were much more frequent in the prevertebral superior mesenteric ganglia than in the paravertebral superior cervical ganglia. These studies demonstrate anatomic, peptidergic, and pathologic specificity in the aging human nervous system similar in many respects to that which the authors have described in experimental animal models. Neuroaxonal dystrophy in the sympathetic nervous system may underlie poorly understood alterations in clinical autonomic nervous system function that develop with age.
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PMID:Neuroaxonal dystrophy in aging human sympathetic ganglia. 169 57

Immunohistochemical methods were used to determine the localisation of immunoreactivities to a variety of antigens involved in neurotransmission in the myenteric plexus of the colon in the rat and mouse. The findings in the two species were closely similar. Five neuronal types have been identified. (i) The axons of extrinsic noradrenergic sympathetic neurons, immunoreactive for tyrosine hydroxylase, supply the ganglia and the circular muscle. (ii) Bombesin immunoreactive intrinsic neurons with unbeaded axons are largely confined to the ganglia and tracts of the plexus. These neurons probably contain gastrin-releasing peptide, which is the mammalian analogue of bombesin. (iii) Somatostatin immunoreactive intrinsic neurons have long, beaded axons within the myenteric plexus and also outside the plexus, between the longitudinal and circular muscle layers. (iv) Intrinsic neurons containing opioid peptides (beta-endorphin, met-enkephalin, leu-enkephalin), have beaded axons that cannot be traced for long distances. They contact all the cell bodies in the ganglia and extend also into the interganglionic tracts and the smooth muscle. (v) Substance P immunoreactive somata and axons are present throughout the myenteric plexus and provide dense innervation to the smooth muscle. Extrinsic substance P immunoreactive sensory axons are probably also present.
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PMID:An immunohistochemical study of the myenteric plexus of the colon in the rat and mouse. 170 22

The outer cortex of the human thymus contains a one- to two-cell-thick layer that is immunoreactive with antisera against beta-endorphin, (Leu)- and (Met)-enkephalin, bombesin, and substance P. The epithelial nature of these immunostained cells is revealed by immunoelectron microscopic studies showing the presence of desmosomal junctions. The presence of peptide-containing cells in the outer cortex, where the most immature and recently immigrated thymocytes are found, emphasizes the role of neuropeptides in regulating the microenvironment for T cell development.
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PMID:Neuropeptide-immunoreactive cells in human thymus. 170 21

Food intake can be increased or decreased after either central or peripheral administration of peptides. Galanin, neuropeptide Y, opioid peptides, growth-hormone-releasing hormone, and desacetyl-melanocyte stimulating hormone increase food intake whereas insulin, glucagon, cholecystokinin, anorectin, corticotropin-releasing hormone, neurotensin, bombesin, cyclo-his-pro, and thyrotropin-releasing hormone reduce food intake. Many of these peptides have reciprocal effects on food intake and sympathetic activity with those peptides that stimulate food intake reducing sympathetic activity and vice versa. In addition, neuropeptide Y specifically increases carbohydrate intake. Galanin and opioid peptides on the other hand increase fat intake whereas enterostatin reduces fat intake. Glucagon decreases protein intake. The effect of peptides on specific nutrients suggests that peptides may work in part by modulating basic feeding mechanisms to lead to the selection of specific nutrients from the diet. This hypothesis might be called a nutrient-specific model of peptide-induced food intake.
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PMID:Peptides affect the intake of specific nutrients and the sympathetic nervous system. 172 38

The effect of bombesin on the activity of dopamine (DA) neurons comprising the nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophysial systems in the male rat was determined by measuring: (1) the accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of a decarboxylase inhibitor, and (2) the concentration of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in brain (striatum, nucleus accumbens, median eminence) and pituitary regions (intermediate and neural lobes) containing terminals of these neurons. Intracerebroventricular (i.c.v.) injection of bombesin caused a dose- and time-related increase in the activity of DA neurons projecting to the median eminence and intermediate lobe of the pituitary, and a corresponding decrease in the concentrations of prolactin and alpha-melanocyte-stimulating hormone (alpha MSH) in the plasma. In contrast, doses of bombesin up to 10 ng i.c.v. failed to alter the activity of DA neurons terminating in the striatum, nucleus accumbens or neural lobe of the pituitary gland. Equimolar doses of bombesin and gastrin-releasing peptide (GRP), a bombesin-like peptide, increased the concentrations of DOPAC in the median eminence and intermediate lobe of the pituitary, suggesting that GRP-preferring receptors may be responsible for the stimulatory effects of bombesin on DA neuronal activity in these regions. The results of these studies suggest that bombesin increases the activity of tuberoinfundibular and tuberohypophysial DA neurons projecting to the median eminence and intermediate lobe of the pituitary, respectively, and thereby inhibits the secretion of prolactin and alpha MSH.
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PMID:Activation of tuberoinfundibular and tuberohypophysial dopamine neurons following intracerebroventricular administration of bombesin. 177 50

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.
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PMID:Temporal relations of the endocrine response to exercise. 187 87

In the present study we examined the effect of the two endogenous opioids met-enkephalin and met-enkephalin Arg6Phe7 on gastric bombesin-like immunoreactivity, gastrin and somatostatin release. At doses of 10(-11), 10(-9), 10(-8) and 10(-6) M both peptides elicited a significant stimulation of bombesin-like immunoreactivity secretion, while the same doses of morphine were ineffective. The stimulatory effect was abolished by naloxone. Met-enkephalin and met-enkephalin Arg6Phe7 stimulated somatostatin secretion at a dose of 10(-8) M, and this effect was reversible by naloxone. Neither peptide had any effect on gastrin secretion. In conclusion, the data demonstrate that both enkephalins must be considered potential regulators of bombesin-like immunoreactivity secretion in the rat stomach.
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PMID:Effect of met-enkephalin and met-enkephalin-Arg6-Phe7 on bombesin-like immunoreactivity (BLI), somatostatin and gastrin secretion from the perfused rat stomach. 197 Dec 49

Central neurotransmitter and/or neuromodulator candidates reported to affect gastric acid secretion are: (excitatory) acetylcholine, thyrotropin releasing hormone, GABA, oxytocin; (inhibitory) noradrenaline, adenosine, bombesin, calcitonin-gene related peptide, corticotropin releasing factor, beta-endorphin, neurotensin, neuropeptide Y, insulin-like growth factor II and prostaglandins. Regulation of gastric acid secretion by central administration of these substances in experimental animals such as rats and dogs are briefly reviewed, and central inhibitory mechanisms of this function are discussed based on our studies with noradrenaline and bombesin. Roles of hypothalamic nuclei such as the ventromedial nucleus and the lateral hypothalamus in regulation of autonomic nerve activities are also described as an introductory note.
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PMID:[Central neurotransmitters and regulation of gastric acid secretion]. 198 Jun 59


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