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)

In the turtle retina the peptides met-enkephalin (metENK), somatostatin (SS), neurotensin (NT), and the indoleamine serotonin (5-HT) modulate ganglion cell (GC) activity. The predominant action of the peptides is excitatory, generally enhancing spontaneous firing and light-evoked activity. In contrast, 5-HT usually inhibits these GC activities. MetENK has both direct synaptic input onto GC and indirect action possibly via a GABA inhibitory interneuron. The metENK actions appear mediated via a mu-opiate receptor; morphine and D-ala-metENK-amide (DALA), a stable analog of metENK, are agonists. Naloxone antagonizes the actions of metENK and its agonists. DALA occasionally inhibits GC. This inhibition is antagonized by picrotoxin, while concurrent excitatory action on GC is enhanced. DALA enhances GC response at high spatial frequencies; naloxone attenuates it. The enhancement by DALA suggests a narrowed receptive-field (RF) center, possibly due to changes in a GABA-mediated inhibitory surround. 5-HT inhibitory actions are also mediated via direct and indirect synaptic pathways. 5-methoxy-dimethyl-tryptamine and methoxy-phenyl-piperazine are agonists of 5-HT action. They are both specific 5-HT1 agonists. LSD (lysergic acid diethylamide) and cyproheptadine, which act on 5-HT2 receptors, antagonize 5-HT actions in this retina. Strychnine enhances GC activity, probably by antagonizing glycine-mediated inhibitory inputs. It does not block the inhibitory action of 5-HT, which suggests that the indirect 5-HT inhibition is not mediated via a glycinergic interneurone. 5-HT suppresses directional selectivity (DS) and attenuates high spatial frequencies in some GC. This may be mediated via inhibition of GABAergic amacrines subserving DS and the RF inhibitory surround.
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PMID:Pharmacological actions of peptides and indoleamines on turtle retinal ganglion cells. 257 68

1. D-ala2-methionine enkephalinamide (DME), the stable analogue of met-enkephalin (an opioid agonist), stimulated food intake of immature hens in the first 30 min after intracerebroventricular injection (2 and 8 micrograms/kg), but had no effect on either food or water intake when injected intravenously (15 and 60 micrograms/kg). 2. Naloxone (an opioid antagonist) had no effect on food intake after either intracerebroventricular (50 and 200 micrograms/kg) or intravenous (1 and 4 mg/kg) injection, but inhibited water intake in the second 30 min after intravenous injection. 3. Water intake was not measured after the intracerebroventricular injections of DME and naloxone. 4. Both feeding and drinking were inhibited in a dose-related way in the 7 h after intramuscular injection of nalmefene (0.2, 0.4, 0.8 and 1.6 mg/kg), a more potent and longer-lasting antagonist than naloxone. 5. These data are compared with published results from similar work with birds and mammals. It is concluded that central release of endogenous opioids may reinforce both feeding and drinking in fowls, but whereas opioid blockage affects feeding more than drinking in pigeons and quail, the opposite appears to be the case in fowls.
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PMID:Opioid modulation of feeding and drinking in fowls. 276 84

The action of enkephalin-analogues (D-ala2-D-leu5-enkephalin and D-ala2-D-met-enkephalin) and morphine, iontophoretically applied, was tested on rat cortical neurons intracellularly recorded "in vivo". Inhibition of cellular excitability of 60% of the tested cells followed the iontophoretic administration of opioid peptides. 50% of the inhibited cells were also hyperpolarized. The amplitude of membrane hyperpolarization was related to the value of the membrane potential. In 13 out of the 30 inhibited cells the change in membrane input resistance was measured; the input resistance was decreased by 30%. In 8 cells, hyperpolarized by the opioid peptides, the depolarizing postsynaptic potentials, evoked by cortical stimulation, were also reduced in amplitude. Naloxone, iontophoretically applied, reversed and/or prevented the peptide responses. On the same neurons, morphine induced a bursting pattern of spiking activity and increased the membrane input resistance: this action was naloxone-insensitive. The reported results suggest that opioid peptides and morphine activate, respectively, naloxone-sensitive and naloxone-insensitive mechanisms on the same cortical neurons, leading to different and, in some respect, opposite effects on the neuronal activity.
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PMID:Met- and leu-enkephalins inhibit rat cortical neurons intracellularly recorded in vivo while morphine excites them: evidence for naloxone-sensitive and naloxone-insensitive effects. 279 77

Post-training treatment alters memory by different mechanisms. Naloxone enhances memory by antagonism of endogenous beta-endorphin-induced state dependency. Epinephrine facilitates consolidation at low doses and generates state dependency at high doses. Exposure to a session of tones causes retroactive interference through a cognitive effect. The present data show that chronic ethanol ingestion, in rats, inhibited the post-training effect of naloxone and of a high dose of epinephrine on the retention of an inhibitory avoidance task but did not inhibit retrograde interference by a session of tones or retrograde facilitation by a low dose of epinephrine. Therefore, ethanol appears to selectively affect post-training influences related to state dependency.
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PMID:Chronic ethanol ingestion selectively affects memory modulation in rats. 280 74

Isolated rat tail arteries were perfused and vasoconstriction was evoked by electrical field stimulation (2 pulses at 1 Hz every 2 min). The vasoconstriction was depressed by DAGO (IC50 = 611 nM) and beta-endorphin (IC50 = 37 nM). Structuraly analogues and shorter fragments of beta-endorphin were also tested. beta-Endorphin and beta-endorphin-(1-26) were about equipotent whereas the beta-endorphin fragments 1-17, 1-16 and 6-31 were inactive. The potencies of beta-endorphin, beta-endorphin-(1-26), -(1-17) and -(1-16) were not changed in the presence of peptidase inhibitors. Structural analogues such as [D-Ala2]beta-endorphin or [Leu5]beta-endorphin had a somewhat lower potency than beta-endorphin itself. Naloxone 30 nM antagonized the effects of DAGO and beta-endorphin to a similar extent with dissociation constants 3.8 and 3.7 nM, respectively for the antagonist against the agonists. The results support the existence in the rat tail artery of a homogenous population of beta-endorphin-sensitive receptors which may belong to the epsilon-type.
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PMID:Further evidence for the existence of a homogenous beta-endorphin-sensitive receptor population in the rat tail artery. 283 51

To determine whether endogenous opiates have a role in circulatory regulation during mild to moderate exercise, 11 chronically instrumented dogs were exercised on a treadmill up a 6% incline at 2.5 and 5.0 mph, each for 20 min, after treatment with either the opiate receptor antagonist naloxone (1 mg/kg bolus and 20 micrograms.kg-1.min-1 infusion) or normal saline. Naloxone increased plasma beta-endorphin and adrenocorticotropic hormone at rest but had no effect on resting heart rate, aortic pressure, cardiac output, left ventricular time derivative of pressure (dP/dt) and ratio of dP/dt at a developed pressure of 50 mmHg and the developed pressure (dP/dt/P), or plasma catecholamines. Plasma beta-endorphin and adrenocorticotropic hormone increased during exercise. In addition, graded treadmill exercise produced proportional increases in heart rate, cardiac output, aortic pressure, left ventricular dP/dt and dP/dt/P, and blood flow to exercising muscles, right and left ventricular myocardium, and adrenal glands. However, there were no differences in the circulatory responses to exercise between animals receiving naloxone and normal saline. Thus the endogenous opiate system probably does not play an important role in regulating the systemic hemodynamic and blood flow responses to mild and moderate exercise.
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PMID:Effects of naloxone on systemic and regional hemodynamic responses to exercise in dogs. 283 52

A range of biologically different opioid peptides are synthesised as components of three distinct precursors, pro-opiomelanocortin, proenkephalin, and prodynorphin. They interact with a number of receptors which have so far been characterised as mu, delta, kappa, sigma, and epsilon. It is unclear which ligands bind to which receptors under physiological circumstances, but preferential in vitro interactions include enkephalins with delta receptors, dynorphin with kappa receptors, and beta-endorphin with epsilon receptors. Post-translational processing determines which of several opioid products are produced from each precursor, but the identity of the enzymes involved and regulation of processing is unknown. Opioid involvement in the neuroendocrine and cardiovascular systems is reviewed. Naloxone-sensitive opioid mechanisms are implicated in the control of gonadotrophin and adrenocorticotropic hormone secretion and in the hypotension of various types of shock. The investigation of possible dynorphin involvement in neurohypophysial function is taking place because vasopressin and dynorphin A (1-8) have been shown to coexist in the neurosecretory vesicles of magnocellular neurons.
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PMID:Opioid biology: the next set of questions. 286 Aug 88

The rat neurohypophysis contains both opioid receptors and substantial amounts of endogenous opioid peptides. Inhibitory influences of opioids on the secretion of both oxytocin and vasopressin have been described. We have examined the effects of a range of opioid agonists and antagonists with differing relative selectivities towards opioid receptor subclasses on the secretion of oxytocin and vasopressin from the isolated neurohypophysis. Oxytocin and vasopressin release evoked by brief periods of electrical stimulation in control experiments was compared to evoked release in the presence of test compounds. Oxytocin release was depressed approximately 25% by the delta-agonist (D-Ala2, D-Leu5)-enkephalin but not affected by putative kappa-agonists or by beta-endorphin. The use of opioid antagonists revealed a strong inhibition of oxytocin secretion by endogenous opioids released during electrical stimulation. Naloxone, relatively mu-selective, enhanced oxytocin secretion by up to 90% with a half-maximal effect at approximately 10(-6) M. MR2266, a relatively kappa-selective antagonist also enhanced oxytocin secretion but displayed agonist-like activity at high concentrations. ICI 154129, a delta-selective antagonist, was without effect on oxytocin secretion. Vasopressin release was unaffected by any of the agonists tested and not potentiated by antagonists at a range of stimulation frequencies. The data do not support the suggestion of an inhibitory endogenous opioid influence over vasopressin secretion within the neurohypophysis but indicate that an endogenous opioid peptide, possibly acting via mu- or kappa rather than delta-receptors, strongly suppresses the secretion of oxytocin.
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PMID:Effects of opioid agonists and antagonists on oxytocin and vasopressin release in vitro. 286 49

The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. However, both low and high concentrations of metenkephalin stimulated insulin secretion. A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). The metenkephalin-induced insulin secretion was partially, but not completely, blocked by naloxone. Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. Met-enkephalin may, therefore, be a physiologic regulator of pancreatic endocrine secretion.
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PMID:The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. 286 28

We evaluated the development of naloxone-reversible and naloxone-non-reversible analgesia induced by footshock in rats of different ages and correlated it with the concentrations of beta-endorphin and dynorphin in brain areas and the spinal cord. We observed that naloxone-non-reversible shock-induced analgesia appeared first and its appearance might be related to the early presence of high dynorphin concentrations in the spinal cord. Naloxone-reversible analgesia appeared later together with the reaching of adult concentrations of cerebral beta-endorphin.
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PMID:Naloxone-reversible and non-reversible shock-induced analgesia during development. 286 71


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