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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analgesia and locomotor activity are genetically differentiated in C 57 and DBA mice. In fact, DBA strain, unlike C 57, is very sensitive to the analgesic effects of morphine. On the contrary, morphine elicits an increase of locomotor activity only in C 57 mice. We have used this genetic approach to study the in vitro response of vas deferens contractions to morphine and methionine-enkephalin. The results obtained are the following: 1. The percentage of morphine inhibition of the electrically evoked contractions of the longitudinal muscle of the vas deferens is greater in DBA strain, which is sensitive to the analgesic effects of morphine, than in C 57 mice in which morphine exerts a stimulating effect of the locomotor activity; 2. Met-enkephalin has been found to be more active than morphine on the same preparation; 3. The inhibitory effects of Met-enkephalin appear to be greater in C 57 than in DBA mice; 4. Different doses of Naltrexone are required to reverse the effects of morphine and Met-enkephalin; 5. Cumulative doses of Met-enkephalin and morphine induce different responses in the vas deferens of C 57 and DBA mice. The results emphasize the usefulness to study analgesic activity in these strains of mice.
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PMID:Genotype dependent response of morphine and methionine-enkephalin on the electrically induced contractions of the mouse vas deferens. 72 70

Intraseptal administration of morphine (70 nmol) or beta-endorphin (0.7 nmol) reduced the rate of acetylcholine (ACh) turnover (TRACh) in rat hippocampus but not in striatum or cortex. These intraseptal injections failed to modify the ACh content and did not elicit analgesia. Naltrexone (15 mumol/kg, i.p.) completely antagonized the decrease of hippocampal TRACh elicited by the two opiate receptor agonists. Furthermore, intraseptal injections of naltrexone partially blocked the decrease in hippocampal TRACh induced by intraperitoneal administration of morphine (70 mumol/kg, i.p.). These data suggest that opiate agonists decrease hippocampal TRACh by regulating septal cholinergic neurons, and that this effect is not associated with analgesia.
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PMID:Inhibition of acetylcholine turnover in rat hippocampus by intraseptal injections of beta-endorphin and morphine. 90 10

In rats, an ED50 for analgesia of morphine, meperidine, viminol R2 or azidomorphine decreases the turnover rate of acetylcholine (TRACh) in cortex and hippocampus. These four analgetics fail to change to TRACh in striatum when given in a dose range from ED30 for analgesia up to a cataleptic dose. Viminol S2, a nonanalgesic stereoisomer of vimonol R2, fails to decrease the TRACh in cortex and hippocampus. Naltrexone, an opiate antagonist, also fails to change the cortical and hippocampal TRACh but it antagonizes the decrease in cortical and hippocampal TRACh elicited by the four analgetics. Since the ED50 of these four analgetics fails to change the TRACh in striatum which contains a high density of opiate receptors and intrinsic cholinergic neurons, but decreases the TRACh in hippocampus and cortex which contain a low density of opiate receptors, it can be inferred that opiate receptors are not exclusively involved in the regulation of TRACh. However, the results suggest that certain cholinergic pathways participate in the mediation of analgesia.
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PMID:Correlation between analgesia and the decrease of acetylcholine turnover rate in cortex and hippocampus elicited by morphine, meperidine, viminol R2 and azidomorphine. 103 2

The present study was conducted to evaluate the agonist and antagonist properties of kappa opioids in the squirrel monkey shock titration procedure. The opioid antagonist naltrexone, the kappa agonists U50,488, bremazocine, ethylketazocine and tifluadom, and the mu agonist l-methadone were administered alone and in combination with a single dose of the mu agonist morphine. When administered alone, all opioids except naltrexone produced dose-dependent increases in median shock level (the intensity below which monkeys maintained shock 50% of the time). In addition, all kappa agonists produced increases in urine output, whereas naltrexone and l-methadone did not. When combined with morphine, naltrexone and all kappa agonists antagonized, at least partially, morphine-induced increases in median shock level, whereas l-methadone did not. Naltrexone and the four kappa agonists also shifted an l-methadone dose-effect curve rightward in a parallel manner; however, the shifts produced by naltrexone were greater in magnitude than those produced by the kappa agonists. These studies demonstrate that a variety of kappa agonists can act as mu antagonists in a primate model of analgesia, although antagonist activity of kappa opioids appears to be limited by their agonist activity in this procedure. Order of potency among the kappa agonists for analgesic, diuretic and antagonist effects was very similar (bremazocine greater than ethylketazocine greater than tifluadom greater than or equal to U50,488), as was the dose range for peak diuretic and antagonist effects, suggesting that mu antagonism among kappa agonists may be kappa-mediated in the squirrel monkey.
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PMID:Agonist and antagonist activity of kappa opioids in the squirrel monkey: I. Antinociception and urine output. 130 76

Chronic treatment with an opioid antagonist, such as naltrexone, increases opioid receptor density and opioid agonist potency. Since stimulants such as d-amphetamine can increase opioid potency and opioid abusers may administer stimulants during naltrexone treatment, the effect of chronic d-amphetamine on naltrexone-induced opioid receptor upregulation and supersensitivity was examined in mice. Mice were implanted s.c. with a 15 mg naltrexone or placebo pellet for 8 days. Mice were injected daily with saline or d-amphetamine (7.5 or 5.0 mg/kg per day s.c.) for 7 days beginning 24 h following implantation. Naltrexone and placebo pellets were removed on the 8th day, and 24 h later mice were tested for morphine analgesia (tail-flick) or whole brain was removed and opioid receptor binding studies were conducted. Chronic naltrexone significantly enhanced the analgesic potency of morphine in saline-treated mice. However, naltrexone treatment did not increase morphine potency in mice treated with d-amphetamine. In binding studies, naltrexone increased [3H][D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO) Bmax (+60-70%) without altering KD in both saline- and d-amphetamine-treated mice. Results from studies with 2 nM [3H][D-Pen2,D-Pen5]enkephalin (DPDPE) were similar. These studies indicate that daily d-amphetamine can limit naltrexone-induced supersensitivity but not receptor upregulation. Thus, upregulation can be dissociated from functional supersensitivity.
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PMID:Chronic d-amphetamine inhibits opioid receptor antagonist-induced supersensitivity. 133 Jun 22

This study examined the effects of chronic (7 day) administrations of opioid agonists, via osmotic minipumps (20 micrograms/microliters/h, or 2 mg/kg/h for each agent) on: 1) nociception and activity, and 2) the analgesic and locomotor responses of subordinate male mice experiencing social conflict (aggression without defeat) and defeat in a "resident-intruder" paradigm. Chronic infusion of the mu opioid antagonist, naltrexone, resulted in a hypoanalgesic response and a decrease in basal locomotor activity on days 3-7 postimplantation which returned to the basal levels of saline-implanted control mice after termination of the infusions on day 9. Naltrexone reduced defeat-induced analgesia on the second day after implantation, but had no consistent effects on analgesia on test days 6 and 9 or on the aggression-induced (nondefeat) analgesia and increases in activity. The delta opioid antagonist ICI-154, 129, while having no significant effects on basal nociception or locomotor activity, augmented nondefeat-induced analgesia (day 2) and reduced the defeat-induced increases in activity (days 2 and 6). The mu agonist, levorphanol, resulted in a significant analgesia on the first two days after infusion, followed by the development of tolerance to the analgesic effects over days 3-7. On day 9, a hypoanalgesic response indicative of withdrawal was evident. Levorphanol also induced a marked decrease in locomotor activity over days 3-7 postimplantation, with no evidence of the development of tolerance or withdrawal following termination of infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modifications of social conflict-induced analgesic and activity responses in male mice receiving chronic opioid agonist and antagonist treatments. 164 45

The first aim of this study was to test whether opioid mediation of conditional analgesia is inversely related to the relative amount of training that rats received, a prediction derived from the severity hypothesis. Naltrexone attenuated the analgesia among subjects in the low-training group but had no effect in rats given an extended amount of training. The second aim of this study was to investigate whether noradrenergic, opiate, and serotonergic spinal systems play a role in conditional analgesia. Intrathecal administration of yohimbine, an alpha 2 antagonist, completely blocked both opioid and nonopioid forms of conditional analgesia. Spinal administration of either quaternary naltrexone or methysergide failed to have an effect. In addition to providing support for the severity hypothesis, these results indicate that both opioid and nonopioid forms of conditional analgesia are subserved by critical alpha 2-adrenoceptors at the spinal level.
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PMID:Opioid and nonopioid conditional analgesia: the role of spinal opioid, noradrenergic, and serotonergic systems. 166 31

The etiology of the Rett syndrome (RS) is unknown. Reduced function of biogenic amines has been described. Symptoms of central apnea, hyperventilation, hypothermia, peripheral analgesia, muscle rigidity, myoclonic jerks, hand stereotypy and seizures occur in RS and have been suggested as a result of elevated central beta-endorphins. It was hypothesized that a dysfunctional modulation of endogenous opiate systems and biogenic amines may be present. Cerebrospinal fluid (CSF) from 12 girls with RS was studied for beta-endorphin immunoreactivity, and biogenic amines. Lactates and pyruvate levels were measured. Eleven of the 12 girls had elevated beta-endorphin immunoreactivity in CSF, 4 girls had reduced biogenic amines and 6 girls had elevated pyruvate and lactate levels. Whether the elevated beta-endorphin immunoreactivity is a primary disorder or is a result of secondary feedback mechanisms is unknown. Naltrexone, an antiopioid drug, may reduce symptoms.
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PMID:Cerebrospinal fluid studies in the Rett syndrome: biogenic amines and beta-endorphins. 169 44

Previous research has demonstrated that exposure to a cat produces a naltrexone-reversible antinociception as assessed in the formalin test in rats. Because different neurochemical mechanisms inhibit different forms of nociception, the present study examined whether presentation of a cat would also produce a naltrexone-reversible antinociception in the tail-flick response to radiant heat and electric shock. Exposure to the cat produced antinociception in both tail-flick paradigms. Naltrexone blocked the inhibition of the thermally evoked tail-flick response, but had no effect in the electric shock tail-flick paradigm. These results indicate that opioid mediation of stress-induced analgesia is determined, in part, by the nociceptive test employed.
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PMID:Cats produce analgesia in rats on the tail-flick test: naltrexone sensitivity is determined by the nociceptive test stimulus. 208 38

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component. When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 x 10(-3) mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice. These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatobiliary effects of morphine are mediated in the brain. 217 93


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