Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta-Endorphin-(1-27), administered intraventricularly has been previously reported to block the analgesia induced by beta-endorphin injected intraventricularly. The present study was to determine if the blocking effect of beta-endorphin-(1-27) was specific to beta-endorphin which stimulates epsilon receptors, but not to other opioids with activity at different opioid receptors. The antagonistic effects of beta-endorphin-(1-27) on the analgesia induced by beta-endorphin (epsilon-opioid receptor agonist), D-Ala2-NMePhe4-Gly-ol-enkephalin(DAGO) and morphine, (mu-opioid receptor agonists), D-Pen2-D-Pen5-enkephalin(DPDPE) and D-Ala2-D-Leu5-enkephalin(DADLE) (delta-opioid receptor agonists) and U-50, 488H (kappa-opioid receptor agonist) were studied. beta-Endorphin-(1-27) injected intraventricularly, at doses which, when injected alone did not produce analgesia, antagonized the analgesia induced by beta-endorphin given intraventricularly. However, the analgesia induced by DAGO, morphine, DPDPE, DADLE and U-50, 488H given intraventricularly was not antagonized by beta-endorphin-(1-27). The data suggest that beta-endorphin-(1-27) selectively blocks the analgesia induced by the stimulation of epsilon receptors but not by the stimulation of mu, delta, and kappa receptors. The results support the previously proposed hypothesis that beta-endorphin produces its analgesia by stimulating specific epsilon receptors.
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PMID:Beta-endorphin-(1-27) antagonizes beta-endorphin- but not morphine-, D-Pen2-D-Pen5-enkephalin- and U50, 488H-induced analgesia in mice. 297 39

The neurochemical and functional correlates of opioid receptor up-regulation after chronic antagonist administration in vivo and of down-regulation after withdrawal of antagonist were examined. Total brain opioid receptors increased 1.9-fold by day 8 of naltrexone administration, after which no further increase was observed; the newly synthesized or unmasked receptors exhibited an enhanced sensitivity to guanyl nucleotide modulation. Withdrawal from chronic naltrexone treatment resulted in a return to nearly control levels of receptor density and guanyl nucleotide sensitivity in a period of 6 days. These results suggest that up-regulation is accompanied by an increased coupling of the receptors to the inhibitory guanyl nucleotide binding protein (Ni) and that down-regulation involves the dissociation of the receptor/Ni complex. In experiments designed to target opiate receptor subtypes, long-term treatment with naltrexone was found to produce a coordinated up-regulation of brain mu and delta receptors, but did not cause a significant change in the density or affinity of kappa or sigma receptors. These findings indicate that the kappa and sigma opiate receptor classes may be subject to independent control mechanisms. Chronic naltrexone treatment also resulted in an enhanced morphine-induced analgesia. This result indicates that a functional supersensitivity occurs as a result of the selective up-regulation of mu and delta receptors. After withdrawal from naltrexone, supersensitivity to morphine-induced analgesia decreased monotonically and, in parallel to opioid receptor density, to prenaltrexone treatment levels within 6 days. Together, these results suggest a functional significance for antagonist-induced mu and delta opiate receptor up-regulation.
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PMID:Neurochemical and functional correlates of naltrexone-induced opiate receptor up-regulation. 298 11

Human beta-endorphin (beta h-EP) analogs of variable chain lengths have been investigated for their potency in inhibiting analgesia induced by beta h-EP or by the potent opiate etorphine. It was found that beta h-EP-(1-28) inhibits the analgesic effect of beta h-EP and etorphine when co-injected intracerebroventricularly into mice. Antagonism by competition at same opioid receptor subtypes is suggested from parallel shifts of the dose-response curve of etorphine or beta h-EP in the presence of increasing doses of beta h-EP-(1-28). On a molar basis, beta h-EP-(1-28) is nearly 10 times more potent than naloxone. The reduction of the chain length from residues 1-28 to 1-27 lowered the antagonist potency while further reduction of the peptide chain led to a complete loss of inhibitory activity. From comparison of the opioid-receptor binding affinity, analgesic activity and antagonist potency, it is concluded that the C-terminus of beta-EP is critical to the biological efficacy of the molecule and that the antagonist activity of C-terminal deletion analogs is probably mediated through residues 27 and 28.
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PMID:Inhibition of analgesia by C-terminal deletion analogs of human beta-endorphin. 298 29

The motility, pain-threshold and opioid receptor activities of the synaptic membrane in mice showing conditioned suppression of motility were compared with those in mice given only electric footshock. Electric footshock caused analgesia and a decrease in motility, both of which were partially reversed by administration of high doses of naloxone. In contrast, mice exhibited a marked suppression of motility (conditioned suppression) but not analgesia when placed in the same environment 24 hr after the electric footshock in which the animals received the electric footshock. In the electric footshock group, the [3H]-naloxone binding capacity at low affinity site was increased. These results suggest that the increase in [3H]-naloxone binding capacity may play an important role in the behavioral changes of electric footshock group, but not conditioned suppression group.
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PMID:Differences of alteration in opioid systems induced by conditioned suppression and electric footshock in mice. 298 3

The purpose of the present study was to examine in rats the relationship between the age-related decline in an opioid receptor system and the function of the endogenous opioid pain-inhibitory system activated by front-paw shock. Results revealed that the analgesia displayed following front-paw shock declined between 5- to 7-month-old, 15- to 17-month-old, and 22- to 24-month-old age groups. The administration of naloxone significantly attenuated the shock-induced analgesia. Thus, the endogenous opioid pain modulatory system activated by front-paw shock (the nucleus raphe alatus and a descending pathway lying within the dorsolateral funiculus of the spinal cord) declines in function with increasing age. This research also confirms that there is a parallel between the age-related decline in the neurochemical indexes of the opioid receptor system and the function of these receptors in producing analgesia in response to aversive stimulation.
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PMID:Environmentally induced analgesia: an age-related decline in an endogenous opioid system. 298 89

We have investigated the correlation of electric shock-induced behavioral changes and functional alterations of endogenous opioid receptor subtypes. The degree of electric shock-induced behavioral changes, such as analgesia and motor suppression, was dependent on the duration of and time after electric shock application. The electric shock-induced behavioral changes were completely antagonized by naloxone. The apparent development of tolerance to both behavioral effects as a result of successive daily electric shock was different: Tolerance to electric shock-induced analgesia developed after 2 days' successive electric shock application, while tolerance to motor suppression was not observed even after 7 days' successive electric shock application. There was a decrease of [3H][D-Ala2, Met5]enkephalinamide ([3H]DAMEA, delta agonist) binding and an increase of [3H]naloxone (mu antagonist) binding when potent electric shock-induced analgesia developed. On the other hand, the binding of [3H]DAMEA and [3H]ethylketocyclazocine (kappa agonist) was significantly changed when locomotion was suppressed. These results suggest strongly that different opioid systems may participate in electric shock-induced analgesia and motor suppression: electric shock-induced analgesia and motor suppression may be mediated by mu/delta and kappa/delta receptors, respectively.
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PMID:Involvement of different opioid receptor subtypes in electric shock-induced analgesia and motor suppression in the rat. 299 79

Three antagonists at the mu opiate receptor site: naloxone, naltrexone and diprenorphine, and one agonist-antagonist compound nalorphine, at doses usually not analgesic elicited analgesia in rats when administered after non-naloxone-reversible shock-induced analgesia had disappeared. The chi receptor antagonist, MR 2266, and the delta antagonist, ICI 154129, were all ineffective. This effect was no longer present when non-naloxone-reversible shock-induced analgesia was inhibited by the administration of the chi receptor antagonist, MR 2266. These results suggest that the mu opiate receptor may change its conformation under particular conditions such as continuous inescapable shock.
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PMID:Analgesic effects of mu antagonists after naloxone non-reversible stress-induced analgesia. 300 May 23

Morphine-induced analgesia, and the development of morphine-induced tolerance and dependence was determined in mice which had drunk caffeinated water (1 mg/ml) for 14 days or in mice which had received (-)-N6-(phenylisopropyl)-adenosine (PIA) 1 mg/kg i.p. for 14 days. Analgesia was assessed by the tail flick assay. The development of dependence was assessed by determining the ED50 of naloxone to precipitate withdrawal jumping (3 h after 100 mg/kg morphine pretreatment or 72 h after s.c. implantation of a morphine 75 mg pellet) and by determining the extent of naloxone-precipitated hypothermia in morphine-implanted animals. In mice chronically administered caffeine, the ED50 for morphine-induced analgesia was significantly decreased while the naloxone ED50 for withdrawal jumping increased by 2-fold after both types of morphine pretreatment. In control animals (tap water for 14 days), doses of 1 and 10 mg/kg of naloxone caused significant hypothermia in morphine-implanted animals. Doses of naloxone up to 100 mg/kg did not cause significant hypothermia in morphine-implanted animals which had received chronic caffeine. The development of tolerance was determined by computing the morphine potency ratio for the tail flick assay (tolerant ED50/control ED50). In mice chronically administered caffeine, the potency ratio was decreased significantly in morphine-implanted animals when compared to control. Morphine-induced analgesia, tolerance and dependence was not changed significantly in animals chronically administered PIA. Neither the distribution of morphine to the brain nor the opioid receptor binding parameters for [3H]etorphine and [3H]naltrexone were altered in mice chronically administered caffeine or PIA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of chronic administration of caffeine on morphine-induced analgesia, tolerance and dependence in mice. 300

The effects of beta-FNA, a highly selective and irreversible mu opioid receptor antagonist, in altering body and brain development in preweaning rats were determined. Animals given beta-FNA did not differ from controls in body weights, brain and cerebellar weights, macroscopic dimensions of the brain, the area of the cerebellum, or in organ weight. The dosage of beta-FNA utilized (5 mg/kg) blocked morphine-induced analgesia (2 mg/kg morphine sulfate, SC) for each injection period (i.e., 48 hr). In contrast to beta-FNA treatment, rats given naltrexone (50 mg/kg SC) in a regimen which completely blocked the opioid receptor throughout ontogeny exhibited marked increases in somatic and neurobiological growth. These results suggest that, in and by themselves, mu receptors selectively antagonized by beta-FNA do not play an important role in regulating development.
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PMID:beta-Funaltrexamine (beta-FNA) and the regulation of body and brain development in rats. 301 87

Prenatal stress affects the expression of many opioid-regulated behaviors in adulthood, e.g., aggressive, maternal, regulatory, and sexual. In the present report we examined two forms of analgesia, morphine-induced (opioid receptor-mediated), and stress-induced [cold-water swim (CWS), nonopioid] analgesia in adult prenatally-stressed (P-S) male and female rats to determine whether and to what extent these analgesic responses might be altered. Timed-mated Sprague-Dawley females were exposed to heat and restraint stress (three daily 1/2 hour sessions, 0830, 1230, and 1630 hr) from days 15-22 of gestation. Control animals remained undisturbed throughout pregnancy. Between 120-150 days of age, baseline pain sensitivities were determined using a tail-flick monitor. P-S and Control animals were then exposed to 3.5 min cold-water swims (2 degrees C) and pain thresholds were again determined at 30 min intervals for 120 min. P-S females exhibited significantly lower pain thresholds than Control females at the 30 and 60 min marks, whereas P-S and Control males did not differ. Six to eight days later, analgesia was measured for 180 min following morphine (5.0 mg/kg) administration. P-S females exhibited significantly greater analgesia at each time-point after morphine treatment than Controls. Conversely, P-S males were significantly less analgesic than Control males from 60 to 180 min. These data suggest that prenatal stress alters the status of endogenous opiate systems. Such prenatal stress-induced alterations in opiate function may help account for some of the behavioral effects reported in P-S animals.
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PMID:Prenatal stress alters morphine- and stress-induced analgesia in male and female rats. 317 33


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