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 effects of beta-endorphin on the antinociceptive responses and abrupt withdrawal jumping in morphine-dependent mice were studied. Mice were rendered morphine dependent by implantation of a morphine pellet (75 mg base) for 3 days. The analgesic response to beta-endorphin decreased after morphine pellet implantation, as evidenced by an eight-fold increase in the median antinociceptive dose of morphine was found. In small doses (0.09-0.17 mug per mouse), beta-endorphin suppressed abrupt withdrawal jumping. Met-enkephalin, even in high doses (200 mug per mouse), did not suppress abrupt withdrawal jumping.
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PMID:beta-Endorphin: cross tolerance to and cross physical dependence on morphine. 18 88

The intracerebroventricular (i.c.v.) injection of antisera directed against different sequences of Gs alpha to mice enhanced the antinociceptive potency of the opioids morphine, beta h-endorphin-(1-31) and of the alpha 2-agonist clonidine when studied 24 h later in the tail-flick test. The activity of DAGO, DADLE, DPDPE and [D-Ala2]-Deltorphin II remained unchanged after that treatment. Cholera toxin (0.5 microgram/mouse, i.c.v.), agent that impairs the receptor regulation of Gs transducer proteins promoted comparable changes in the supraspinal analgesia induced by these substances. Six days after a single i.c.v. injection (0.5 microgram/mouse) of pertussis toxin the antinociceptive activity of all the opioids and clonidine appeared diminished. It is concluded that opioids and clonidine promote analgesia after binding to receptors functionally coupled to Gi/G(o) proteins, moreover, the activity of morphine, beta-endorphin and clonidine in this test seems to be counteracted by a process involving activation of Gs alpha transducer proteins.
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PMID:Intracerebroventricular injection of antibodies directed against Gs alpha enhances the supraspinal antinociception induced by morphine, beta-endorphin and clonidine in mice. 144 47

These studies investigated the effect of met-enkephalin, glycyl-glutamine, and naltrexone on NK cell activity in vivo and in vitro. It was found that both met-enkephalin (which shares the amino-terminal end of beta-endorphin) and glycyl-glutamine (which reflects the carboxyl-terminal end of beta-endorphin) can enhance the NK cell activity of mice prestimulated with a low dose (1 microgram/mouse) of poly I:C. Naltrexone had no effect. In vivo prestimulation of the mice with 1 microgram poly I:C was necessary as mice which were not pretreated with poly I:C did not show enhanced NK cell activity when treated with either met-enkephalin or glycyl-glutamine. In vitro studies however indicate that the drugs when cultured together with the NK cells from mice preactivated with poly I:C did not have a direct stimulatory effect on the NK cells. These studies imply that while beta-endorphin released from the pituitary could be involved in enhancement of activated NK cells in vivo other indirect peripheral pathways might be involved. The results suggest beta-endorphin probably reacts with other accessory type cells which in turn release the mediators which are required for the stimulation of NK cells in vivo.
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PMID:In vivo enhancement of NK cell activity with met-enkephalin and glycyl-glutamine: their possible role in the conditioned response. 180 31

Cholera toxin, an agent that impairs the function of Gs transducer proteins, was injected (0.5 microgram/mouse, icv) and the antinociceptive activity of opioids and clonidine was studied 24h later in the tail-flick test. In these animals, an enhancement of the analgesic potency of morphine, beta-endorphin and clonidine could be observed. Cholera toxin did not modify the antinociception evoked by the enkephalin derivatives DAGO and DADLE. Pertussis toxin that catalyses the ADP ribosylation of alpha subunits of Gi/Go regulatory proteins was given icv (0.5 microgram/mouse). This treatment reduced the analgesic effect of opioids and clonidine. However, while the analgesia elicited by DAGO, DADLE and clonidine was greatly decreased, the effect of morphine and beta-endorphin was reduced to a moderate extent. It is concluded that Gi/Go regulatory proteins functionally coupled to opioid and alpha 2 receptors are implicated in the efficacy displayed by opioids and clonidine to produce supraspinal analgesia. Moreover, these two receptors are susceptible to regulation by a process that might involve a Gs protein.
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PMID:Cholera toxin and pertussis toxin on opioid- and alpha 2-mediated supraspinal analgesia in mice. 185 Apr 93

CD-1 mice were trained in a classically conditioned emotional response paradigm and tested 24 hr later. Exposure to an open field 0 or 1, but not 3 hr after training retroactively interfered with retention of the conditioned emotional response. The retroactive interference was counteracted by the pretest IP administration of beta-endorphin (0.05 microgram/mouse) or epinephrine (1 microgram/mouse), but not by that of oxotremorine (5 micrograms/mouse). The three drugs were able to enhance retention test performance in animals not exposed to the open field after training. In view of evidence in the literature that beta-endorphin and epinephrine are released during training in an aversive task like this, it seems likely that these two agents were able to overcome the effect of retroactive interference by reinstating neurohumoral attributes of the conditioned emotional task at the time of testing.
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PMID:Pretest beta-endorphin and epinephrine, but not oxotremorine, reverse retrograde interference of a conditioned emotional response in mice. 253 21

Mice were trained in a step-through inhibitory avoidance task with a 0.6-mA, 60-Hz, 2-s footshock and were tested for retention 3 or 6 hr later. Posttraining intraperitoneal administration of a high dose (25.0 micrograms per mouse) of epinephrine (Epi) impaired retention; this effect was counteracted by another injection of the same dose of Epi given before retention testing either 3 or 6 hr after training. When administered before the 6-hr test but not the 3-hr test, however, Epi enhanced retention (i.e., above that of controls). The retention enhancement, but not the reversal of impairing effects of posttraining Epi, was antagonized by naltrexone (20.0 micrograms per mouse). Naltrexone, when administered alone, had no effect on retention when given before testing. However, posttraining administration of naltrexone produced an enhancement of retention detectable 6 but not 3 hr after training. Furthermore, posttraining naltrexone also blocked the impairing effect of posttraining Epi otherwise seen 6 hr after training. These results suggest that the impairment of retention caused by posttraining Epi is attributable to the induction of state dependency based on an Epi state. When the animals are tested 3 hr after training, this effect appears alone. But, when tested 6 hr after training, the Epi effect appears together with an opioid, presumably beta-endorphin-mediated, state dependency.
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PMID:Retention impairment by posttraining epinephrine: role of state dependency and of endogenous opioid mechanisms. 282 4

The pre-test administration of beta-endorphin (0.05 microgram/mouse), oxotremorine sesquifumarate (5.0 micrograms/mouse), or beta-endorphin plus oxotremorine enhanced retention test performance of a conditioned emotional response in mice. The effects were blocked by scopolamine. Scopolamine had no effect of its own. The data suggest that the retention enhancement caused by beta-endorphin may involve the secondary activation of cholinergic mechanisms.
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PMID:Retention enhancement by pre-test beta-endorphin and oxotremorine and its reversal by scopolamine. 284 8

An excessive insulin releasing effect of adrenocorticotropic hormone (ACTH) and ACTH fragments has been considered as a possible factor contributing to the hyperinsulinaemia of genetically obese hyperglycaemic (ob/ob) mice. To investigate this possibility, plasma glucose and insulin responses of 11- to 14-week-old fed lean and ob/ob mice were examined after intraperitoneal administration of ACTH 1-39, ACTH 1-24 and ACTH 18-39, each at a dose of 25 nmol/mouse (50-115 micrograms/mouse). ACTH 1-39 produced a marked and rapid increase of plasma insulin in both lean and ob/ob mice, the effect being much greater in the ob/ob mutant (maximum increases of 5.5 +/- 1.5 and 46.1 +/- 4.1 ng/ml at 10 min in lean and ob/ob mice respectively, P less than 0.001). In lean mice plasma glucose concentrations showed a protracted decreased (maximum decrease of 3.7 +/- 0.5 mmol/l at 120 min), whereas glucose concentrations were increased (maximum increase of 4.2 +/- 1.3 mmol/l at 60 min) in ob/ob mice. ACTH 1-24 produced qualitatively similar but generally smaller effects than ACTH 1-39, while ACTH 18-39 did not significantly affect glucose and insulin concentrations. In 24 h fasted mice, ACTH 1-39 produced similar but generally smaller effects than in fed mice. The results suggest that the effects of ACTH on glucose and insulin homoeostasis are conferred by the N-terminal 1-24 sequence, and ACTH may exert acute effects which contribute to the hyperinsulinaemia and hyperglycaemia of ob/ob mice.
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PMID:Insulin releasing effects of adrenocorticotropin (ACTH 1-39) and ACTH fragments (1-24 and 18-39) in lean and genetically obese hyperglycaemic (ob/ob) mice. 303 65

Prolyl-leucyl-glycinamide (PLG) at a low dose (10 ng/mouse) administered by an intracerebroventricular (i.c.v.) injection did not affect levorphanol analgesia, but PLG at higher doses (10 and 100 micrograms/mouse) and alpha-melanocyte-stimulating hormone (alpha-MSH) (10 ng/mouse) antagonized levorphanol analgesia. Development of levorphanol tolerance was facilitated by 10 ng/mouse of PLG, unaffected by 10 micrograms/mouse of PLG, but antagonized by 100 micrograms/mouse of PLG and 10 ng/mouse of alpha-MSH. The effect of PLG on levorphanol dependence was assessed by changes in body weight and temperature during naloxone-induced withdrawal. PLG (10 ng/mouse) facilitated the development of levorphanol dependence, but 10 micrograms/mouse of PLG had no effect. PLG (100 micrograms/mouse) antagonized development of levorphanol dependence. PLG at doses of 10 and 100 micrograms/mouse precipitated withdrawal in levorphanol-dependent mice. alpha-MSH (10 ng/mouse) antagonized development of levorphanol dependence as evidenced by an increase in the ED50 of naloxone required to induce withdrawal jumping. These results indicate that PLG and alpha-MSH affected levorphanol-induced analgesia, tolerance and dependence in a qualitatively similar manner to their effect on morphine-induced analgesia, tolerance and dependence.
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PMID:Effect of prolyl-leucyl-glycinamide and alpha-melanocyte-stimulating hormone on levorphanol-induced analgesia, tolerance and dependence. 614 83

In the tail-flick test in mice, the intraventricular administration of Substance P (10-5,000 ng/mouse) produced a naloxone-reversible analgesic effect of rapid onset and long duration. The dose-response curve was bell-shaped, the analgesic effect being smaller after the largest doses. The analgesia was blocked by concomitant intraventricular administration of the antibody against met-enkephalin but not by the antibody against beta-endorphin. In the hot plate assay, Substance P produced analgesia in mice with high sensitivity to pain, and hyperalgesia in mice with lower sensitivity to pain than normal. The analgesia was blocked by the antibody against met-enkephalin but the hyperalgesia or the scratching response were not modified by the antiserum. The results appear to indicate a dual effect, analgesic or hyperalgesic, of Substance P in mice, the former probably being mediated by release of met-enkephalin.
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PMID:Blockade by met-enkephalin antiserum of analgesia induced by substance P in mice. 618 74


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