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)

Morphine, beta-endorphin, Met-enkephalin, and Leu-enkephalin antagonized intestinal actions of cholecystokinin octapeptide (CCK-8), caerulein, and pentagastrin in a manner partly suggesting physiologically competitive antagonism. Further, these acidic peptides (CCK-8, caerulein, pentagastrin) were much more sensitive to the actions of opioids than was angiotensin. Tetrodotoxin also caused changes in the concentration-effect curves, but these were different from the shifts due to the opioids and differentiated between CCK-8, caerulein, and pentagastrin. Naloxone did not modify the response to CCK-8 and caerulein, but completely abolished the antagonistic influence of the opioids. The potencies of morphine and the opioid peptides as antagonists of CCK-8, were of nearly the same order of magnitude. This and the presence in gut and brain of both CCK-like and opioid peptides suggests the hypothesis that these two groups of peptides interact on both myenteric and central nervous system receptors, and thus are directly involved in the regulation of both intestinal motility and satiety.
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PMID:Antagonism of cholecystokinin-like peptides by opioid peptides, morphine or tetrodotoxin. 52 Apr 18

Beta-endorphin (4 micrograms) injected i.v.t. induced the release of immunoreactive [Met5]enkephalin and sulfated cholecystokinin octapeptide (CCK-8s) from the spinal cord in the pentobarbital-anesthetized rat. The inhibition of the tail-flick response induced by beta-endorphin given i.v.t. was antagonized by i.t. injection of CCK-8s and potentiated by i.t. administration of the antibody to CCK-8s. The findings give support to the hypothesis that endogenous CCK-8s in the spinal cord may play a negative feedback role in modulating beta-endorphin-induced antinociception.
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PMID:Release of immunoreactive [Met5]enkephalin and cholecystokinin from the spinal cord by beta-endorphin administered intraventricularly in the pentobarbital-anesthetized rat. 139 96

Mice, partially trained to avoid footshock in a T-maze, showed enhanced retention relative to vehicle-injected mice when treated peripherally with arecoline, D-amphetamine, cholecystokinin octapeptide (CCK-8), epinephrine or naloxone. Both intra-amygdaloid and intraventricular injections of beta-endorphin resulted in amnesia. D-amphetamine and arecoline blocked the amnestic effect of beta-endorphin administered into the amygdala but it required higher doses for CCK-8, epinephrine and naloxone to block the amnestic effect of beta-endorphin. The effects of CCK-8, epinephrine and naloxone showed a differential ability to block amnesia induced by beta-endorphin intraventricularly with epinephrine and naloxone preventing amnesia but CCK-8 not improving retention. This data suggests that the memory enhancement produced by peripherally administered CCK-8 involves the amygdala and that both CCK-8 and epinephrine interact with opioid amnestic mechanisms within the amygdala to alter memory processing.
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PMID:Evidence that cholecystokinin-enhanced retention is mediated by changes in opioid activity in the amygdala. 151 38

The effects of sulfated cholecystokinin octapeptide (CCK8s) given intrathecally (i.t.) or intracerebroventricularly (i.c.v.) on inhibition of the tail-flick and paw-licking hot-plate responses induced by beta-endorphin, morphine, D-Ala2-N-Me-Phe4-Gly-ol-Enkephalin (DAMGO) and D-Pen2-D-Pen5-Enkephalin (DPDPE), given i.t. or i.c.v., were studied in male ICR mice. CCK8s (1 ng) given i.t. effectively antagonized inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin (2 micrograms) and DPDPE (10 micrograms) but not morphine (4 micrograms) or DAMGO (0.02 microgram). However, CCK8s given i.t. did not affect inhibition of the hot-plate response induced by any of the opioid agonists. CCK8s (0.2-40 ng) in combination with beta-endorphin (2 micrograms) or morphine (4 micrograms) given i.c.v. did not affect beta-endorphin- or morphine-induced inhibition of the tail-flick and hot-plate responses. CCK8s and its fragments given i.t. attenuated i.c.v. beta-endorphin-induced tail-flick inhibition with different potencies and efficacies. CCK8s was the most potent compound in antagonizing i.c.v. beta-endorphin-induced tail-flick inhibition. The rank order of potencies was CCK8s greater than CCK(27-33) much greater than caerulein. All three compounds were efficacious, whereas CCK(30-33) was not, in antagonizing beta-endorphin-induced tail-flick inhibition. Intrathecal administration of CCK8s (1 ng) significantly attenuated the tail-flick inhibition induced by i.t. beta-endorphin (0.5-1 microgram) and DPDPE (5 micrograms) but not morphine (0.5-1 microgram), DAMGO (5 ng), norepinephrine (5 ng) or serotonin (16 micrograms).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholecystokinin administered intrathecally selectively antagonizes intracerebroventricular beta-endorphin-induced tail-flick inhibition in the mouse. 154 80

Studies performed in conscious female rats confirmed that iv injection of cholecystokinin octapeptide (CCK; 20 mu/kg) increased the circulating concentration of oxytocin but not that of vasopressin, and confirmed that the stimulation of oxytocin release was markedly facilitated after iv administration of naloxone (1 mg/kg), indicating attenuation of oxytocin release by endogenous opioids. To investigate the site of action of the endogenous opioids, the electrical activity of putative oxytocin neurones in the supraoptic nucleus was recorded in urethane-anaesthetised female rats. Oxytocin neurones responded to CCK injection with an increase in firing rate lasting 5-15 min, but this response was not facilitated by prior injection of naloxone. The results suggest that the opioid influence upon CCK-induced oxytocin release operates at the level of the neurosecretory terminals in the neurohypophysis rather than centrally. Since CCK does not elevate vasopressin release, it appears unlikely that dynorphin, the opioid peptide co-existing with vasopressin, is responsible in these circumstances for the cross-inhibition of oxytocin release. It is suggested that products of proenkephalin A, the met-enkephalin precursor present in the supraoptic nucleus and in the neurohypophysis itself, may be active in the regulation of oxytocin release.
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PMID:Naloxone potentiates the release of oxytocin induced by systemic administration of cholecystokinin without enhancing the electrical activity of supraoptic oxytocin neurones. 157 6

A reverse-phase, high-performance liquid chromatographic (HPLC) method was employed to separate and characterise five neuropeptides from complex mixtures, with important advantages over methods employed earlier using combined HPLC-RIA studies. Peptides were separated using 0.5M pyridine-0.5M formic acid buffer, pH 4, containing propan-l-ol 14% (met-enkephalin, leu-enkephalin, neurotensin) or 20% (CCK-8-S, substance P) at a flow rate of 1.0 ml/min. Isocratic conditions, and volatile solvents, resulted in a highly reproducible method, producing samples in a form designed for subsequent RIA. The application and importance of the procedure is demonstrated by comparison of the measurements of apparent peptide levels in crude brain extracts with those of authentic peptides as determined after HPLC purification.
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PMID:Isocratic reverse-phase HPLC separation and RIA used in the analysis of neuropeptides in brain tissue. 172 86

Recent work has shown that infusions of beta-endorphin, an endogenous opioid, into the ventricular system of lactating rats blocks normal maternal behavior. Other behavioral and biochemical studies have demonstrated that sulfated cholecystokinin-octapeptide (CCK-8) can have effects opposite those of opioids. The present study evaluated whether intracerebroventricular (ICV) administration of CCK-8 is able to antagonize the inhibitory effect of beta-endorphin on maternal behavior. The results of this study demonstrated that CCK-8 (14.5 nmol) prevented the beta-endorphin (1.45 nmol)-induced increase in latencies to retrieve the first pup, retrieve all pups, and to group and crouch over rat pups. In addition, reductions in the percentage of rats retrieving all pups and displaying full maternal behavior were prevented by CCK-8. These data suggest that CCK-8 can act as an opioid antagonist in neural systems that control maternal behavior.
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PMID:Intracerebroventricular cholecystokinin infusions block beta-endorphin-induced disruption of maternal behavior. 192 4

Subcutaneous (sc) administration of 200 micrograms/kg ceruletide (CER), a decapeptide chemically related CCK-8, and 5 mg/kg haloperidol (HLP) to rats increased the plasma immunoreactive beta-endorphin (ir-beta-END) level. The combined injection of CER and haloperidol caused higher plasma ir-beta-END levels than either drug alone. High plasma ir-beta-END levels returned to control levels on the 2nd day. Prior intraperitoneal (ip) administration of a CCK receptor antagonist, L-364,718 (3 mg/kg), but not proglumide (400 mg/kg, ip), inhibited CER-induced, but not HLP-induced, elevation in plasma ir-beta-END levels. The dopamine agonist, bromocriptine (1 mg/kg, ip) decreased plasma ir-beta-END levels, but had not effect on CER-induced elevation in plasma ir-beta-END levels, whereas bromocriptine-induced reduction in plasma ir-beta-END levels was antagonised by HLP. CER injection to chronically HLP-treated rats caused a greater elevation of plasma ir-beta-END levels compared to saline-injected rats. In contrast to the acute experiment, plasma ir-beta-END levels remained elevated over a period of 24 h. In the acute experiment, CER, HLP or the combined treatment with these two drugs had no effect on ir-beta-END contents in the pituitary gland and brain. In the chronic experiment, HLP increased the adenohypophyseal and septal ir-beta-END contents and decreased the hippocampal ir-beta-END contents 24 h after the final HLP injection. CER caused a small reduction only in the hippocampal ir-beta-END contents of CER-injected rats 15 min after injection. When determined on the 2nd day, however, the increases in the adenohypophyseal and septal ir-beta-END contents and the decrease in the hippocampal ir-beta-END contents observed in CER-injected rats were of the same magnitude as those of rats not given the CER injection. These findings indicate that CER stimulates the release of ir-beta-END from the adenohypophysis through CCK-A receptors and that elevated plasma ir-beta-END levels is partly involved in some behavioural effects induced by CER. Furthermore, sustained elevation of plasma ir-beta-END levels after a single injection of CER to chronically HLP-treated rats may explain its long-lasting therapeutic and behavioural effects.
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PMID:Effects of ceruletide and haloperidol on the hypothalamo-pituitary beta-endorphin system and brain beta-endorphin contents in the rat: with special reference to effects of ceruletide in chronically haloperidol-treated rats. 204 84

The effects of sulfated cholecystokinin octapeptide (CCK-8s) and CCK-8s antagonist, proglumide, given intrathecally (i.t.) on inhibition of the tail-flick and hot-plate paw-licking responses induced by beta-endorphin and morphine given intracerebroventricularly (i.c.v.) were studied in male ICR mice. Both CCK-8s (up to 0.5 ng) and proglumide (up to 10 micrograms) injected alone did not affect significantly the control latencies of the tail-flick and paw-licking responses. I.t. injection of CCK-8s as doses from 0.125 to 0.5 ng dose dependently attenuated inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin. The antagonistic effect of CCK-8s on beta-endorphin-induced inhibition was blocked by the co-i.t. injection of proglumide (0.1-1 micrograms) in a dose-dependent manner. High doses (2.5-10 micrograms) of proglumide given i.t. dose dependently enhanced inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin. However, i.t. injection of CCK-8s and proglumide did not affect inhibition of the paw-licking response induced by i.c.v. administered beta-endorphin. The inhibitions of the tail-flick and paw-licking responses induced by i.c.v. administered morphine were not affected by i.t. injection of CCK-8s or proglumide. Our results suggest that CCK-8s in the spinal cord may play an important modulatory role in attenuating the descending pain inhibition induced by i.c.v. administered beta-endorphin but not morphine.
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PMID:Differential effects of sulfated cholecystokinin octapeptide and proglumide injected intrathecally on antinociception induced by beta-endorphin and morphine administered intracerebroventricularly in mice. 214 90

The presence and distribution of regulatory peptides in nerves and endocrine cells of the stomach, intestine and rectum of a urodele amphibian, the mudpuppy, Necturus maculosus, was studied immunohistochemically in sections or whole-mount preparations of the gut wall. The effect of the occurring peptides on gut motility was studied in isolated strip preparations of circular and longitudinal smooth muscle from different parts of the gut. Bombesin-, neurotensin-, substance P- and VIP-like immunoreactivity was present in abundant nerve fibres in the myenteric plexus of both stomach, intestine and rectum. Single fibres or bundles were present in the circular muscle layer and in a well-developed deep muscular plexus in the intestine and rectum. Immunoreactive nerve cells were found in the myenteric plexus of the stomach, intestine (neurotensin only) and rectum. Gastrin/CCK-like immunoreactivity was observed only in a few fibres in stomach and rectum. Endocrine cells containing bombesin-, met-enkephalin-, gastrin/CCK-, neurotensin-, somatostatin- or substance P- like immunoreactivity were present in the mucosa. The effect of bombesin was an inhibition of the rhythmic activity in circular muscle preparations and in longitudinal muscle from the rectum, while longitudinal muscle from the stomach usually responded with a weak increase in tonus. Neurotensin, like-bombesin, was inhibitory on the spontaneous rhythmic activity of circular muscle throughout the gut, while the effect on longitudinal muscle was an increase in tonus. Met-enkephalin and substance P increased the tonus of all types of preparations, and often, in addition, initiated a rhythmic activity superimposed on this maintained tonus. VIP had a general inhibitory effect on the preparations, decreasing tonus and/or abolishing rhythmic activity. It is concluded that bombesin-, neurotensin-, substance P- and VIP-like peptides are present in nerves throughout the urodele gut and may have physiological functions in regulating the motility of the gut. The gastrin/CCK-like peptide present in nerves of the stomach and rectum may affect the function of these parts of the gut. The regulatory peptides present in endocrine cells may, perhaps with the exception of the somatostatin-like peptide, affect the motility humorally.
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PMID:Neuropeptides in the gastrointestinal canal of Necturus maculosus. Distribution and effects on motility. 241 14


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