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)

1. Four different strains of mice were used to study the influence of psychogenetics in opiate tolerance and abstinence. 2. The CD1 strain seemed to be more sensitive to naloxone administration after four days of morphine implantation, because administration of the antagonist induces a number of jumps in the withdrawal phase higher than in the case of the DBA or C3H strains. 3. DBA and C3H mice elicit analgesia before the CD1 strain, whereas the C3H mice lose body weight at a faster rate than the other strains. 4. C57 bl mice died after morphine implantation (100%). 5. These findings are discussed in relation with neurochemical and receptor variations.
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PMID:Influence of psychogenetics in opiate tolerance and abstinence in mice. 193 7

In this paper, the interactions between opiates and antihistaminic compounds, both H1- and H2-blockers, were studied. CD1 mice were used, treated with saline, morphine CHl (5 mg/kg), and 1 or 10 mg/kg of the H1-antihistaminics tripelennamine, chlorpheniramine, diphenhydramine and cyclizine and the H2-antihistaminics ranitidine and cimetidine, all compounds by s.c. route. Using the hot-plate test, it was observed that the two doses of tripelennamine and the higher doses of chlorpheniramine and cimetidine had antinociceptive activity. This increase on analgesia was also observed after chronic treatment with all H1-antihistaminics (10 mg/kg, 3 times daily for 4 days). When antihistaminics were administered with morphine, it was observed that only ranitidine (10 mg/kg) blocked opiate analgesia. On the other hand, previous administration of the opiate antagonist naloxone (1 mg/kg) blocked the antinociceptive action of tripelennamine and chlorpheniramine (10 mg/kg) in control mice. In morphine-dependent mice (by s.c. implantation of a 75-mg morphine pellet), a single injection of diphenhydramine or ranitidine blocked the analgesic action of morphine. Chronic administration of all antihistaminics did not modify morphine analgesia. These data are discussed in relation to the possible binding to the opioid receptors by antihistaminics and their facility in crossing the blood-brain barrier.
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PMID:H1- and H2-histamine receptor blockers and opiate analgesia in mice. 198 58

The role of mu and delta opioid receptors in the spinal and supraspinal analgesic actions of morphine and [D-Pen2, L-Pen5] enkephalin were examined in the tail-flick test utilizing the mu opioid receptor deficient CXBK mouse and BALB/cBy and C57BL/6By, the progenitor strains of CXBK. The analgesic effects of i.c.v. administered morphine were equivalent in the CRS-CD1 (Swiss) standard laboratory mice and the progenitor strains of CXBK. Morphine did not, however, produce analgesia in the CXBK mice at doses greater than 10 times the ED50 dose in the progenitor strains. Similarly, the analgesic effect of i.c.v. [D-Ala2, NMePhe4, Gly-ol]enkephalin, a highly selective mu receptor peptide agonist, also was reduced greatly in the CXBK mice. These data are consistent with the deficiency in mu opioid receptors observed autoradiographically in this strain. In contrast, the highly selective delta opioid receptor peptide agonist [D-Pen2, L-Pen5]enkephalin was equipotent i.c.v. in the CXBK mice and in the progenitor strains of CXBK. In contrast to the effects produced by i.c.v. administration, the analgesic effects of intrathecally administered morphine were similar between CRS-CD1 and CXBX strains of mice. These results suggest that 1) both mu and delta opioid receptors can mediate supraspinal analgesia and 2) that the receptor(s) involved in spinally mediated analgesia is (are) quite distinct from those involved supraspinally.
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PMID:Examination of the involvement of supraspinal and spinal mu and delta opioid receptors in analgesia using the mu receptor deficient CXBK mouse. 283 33

Systemic administration of naloxone usually produces either hyperalgesia or no change in nociception depending on the animal species used and/or the pain test employed. This study, however, demonstrates that naloxone produces a dose-dependent analgesia in the formalin pain test using an inbred strain of albino mouse. Female BALB/c, C57BL/6 and CD1 mice were injected subcutaneously with naloxone HCl in saline (0.1 10.0 mg/kg) or saline alone, and tested for analgesia using the formalin test. Naloxone produced a statistically significant dose-dependent analgesia in the BALB/c mice, with an ED50 of 0.24 mg/kg and almost total analgesia at doses of 1 mg/kg or greater. No changes in pain behaviour were observed in the C57BL/6 or CD1 strains of mice. We believe this to be the first report of analgesia following administration of doses of naloxone normally used for opioid antagonism. To determine if this effect was specific to the formalin test, the 3 strains of mice were injected subcutaneously with naloxone HCl and tested in the tail-flick test. Naloxone had no analgesic action in this test in any of the strains.
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PMID:Systemic administration of naloxone produces analgesia in BALB/c mice in the formalin pain test. 334 67

Some behavioral effects of prenatal morphine administration were studied in CD1 mice. Two sets of experiments were carried out. In a first set, which was performed during development: (a) measures of postnatal reflexes revealed only a light deficit in tests involving motor control, (b) activity measures showed a significant reduction of spontaneous activity which was evident only in the course of the first postnatal days. In a second set of experiments, in which adult mice were tested for activity, analgesia and passive avoidance learning: (a) no difference was observed, in baseline conditions, between the performances of the mice prenatally exposed to saline and those preexposed to morphine, (b) as compared with controls, enhanced responsiveness to morphine administration (for the activity and passive avoidance measures), and to morphine and stress (for the analgesic measures) were found.
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PMID:Prenatal exposure to morphine in mice: enhanced responsiveness to morphine and stress. 654 Apr 49

Recently, the fentanyl-related compound OHM3295 has been shown to induce a naltrexone-sensitive, dose-related analgesia in CD1 mice. However, unlike morphine or fentanyl, which are potent immunosuppressive drugs, OHM3295 has been found to augment splenic natural killer (NK) activity in a dose-related and naltrexone-reversible manner. The present study investigated the type (delta, kappa or mu) of opioid receptor involved in analgesia and immunomodulation after acute administration of OHM3295. CD1 mice pretreated with beta-funaltrexamine (beta-FNA, 40.0 mg/kg) showed an insignificant induction of analgesia (8.4 +/- 3.7%) after 3.2 mg/kg OHM3295, whereas mice pretreated with vehicle, norbinaltorphimine (10.0 mg/kg) or naltrindole (20.0 mg/kg) exhibited 43.6 +/- 12.6% of maximal analgesia, as determined by the tail-flick latency test. Consistent with previous results, acute administration of OHM3295 (3.2 mg/kg) augmented splenic NK activity (20.7 +/- 3.4 lytic units [LU]) relative to vehicle-treated mice (8.2 +/- 0.7 LU). Pretreatment with beta-FNA (40.0 mg/kg) completely blocked (9.0 +/- 1.9 LU) OHM3295-mediated augmentation of NK activity, whereas pretreatment with norbinaltorphimine (10.0 mg/kg) partially blocked (15.8 +/- 2.2 LU) the drug-induced effect. However, pretreatment with naltrindole (20.0 mg/kg) did not antagonize OHM3295-induced increases in splenic NK activity but rather further enhanced (32.3 +/- 4.2 LU) the effect. NK-enriched effector cells from OHM3295-treated mice displayed an increase in conjugation with YAC-1 target cells, an increase in the percent killing of target cells and a significant increase in the number of active killer cells compared with NK-enriched effector cells from vehicle-treated mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fentanyl-related 4-heteroanilido piperidine OHM3295 augments splenic natural killer activity and induces analgesia through opioid receptor pathways. 756

The immunoregulatory effects of fentanyl and a fentanyl-related compound, OHM3295, were studied in mice. Male CD1 mice treated with a range of fentanyl doses (0.1-1.0 mg/kg, subcutaneously) showed suppression of splenic natural killer (NK) activity following 0.25-0.50 mg/kg fentanyl dose but not higher (0.75-1.0 mg/kg) or lower (0.1 mg/kg) doses. Fentanyl (0.01-32.0 mg/kg) also induced dose-related analgesia as measured by an increase in tail flick latency; these analgesic effects were antagonized by naltrexone (1.0-10.0 mg/kg). Pretreatment with naltrexone (1.0-3.2 mg/kg) resulted in significant suppression of splenic NK activity following fentanyl (10.0-32.0 mg/kg) administration. In comparison to fentanyl, OHM3295 (3.2-25.0 mg/kg) augmented splenic NK activity in a naltrexone-reversible manner. Similar to fentanyl, OHM3295 (1.0-32.0 mg/kg) also induced a naltrexone-sensitive, dose-related analgesia as measured by an increase in tail flick latency. These results with OHM3295 demonstrate a novel profile of effects which includes naltrexone-sensitive analgesic effects in the absence of immunosuppressive effects. In addition, this is the first reported case in which a compound with opioid analgesic effects has been shown to potentiate natural killer cytolytic activity following in vivo administration.
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PMID:OHM3295: a fentanyl-related 4-heteroanilido piperidine with analgesic effects but not suppressive effects on splenic NK activity in mice. 784 55

A study was undertaken to investigate the relationship between morphine-induced analgesia and immunosuppression after acute administration. In male CD1 mice, morphine (10.0-100.0 mg/kg s.c.) produced a U-shaped immunosuppressive dose-effect curve on splenic natural killer (NK) activity. Morphine also induced dose-related analgesia, as measured by an increase in tail-flick latency during thermal application; these analgesic effects were antagonized by naltrexone (1.0-10.0 mg/kg). In addition, morphine-induced suppression of splenic NK activity was antagonized in a dose-dependent manner and, at one dose of naltrexone (10.0 mg/kg), splenic NK activity was augmented. To investigate further the relationship between naltrexone antagonism of morphine-induced analgesia and immunomodulation, single doses of morphine (10.0-100.0 mg/kg) were administered to mice pretreated with naltrexone (0.01-10.0 mg/kg) or saline. A dose of 10.0 mg/kg of morphine produced 35% of the maximal possible effect in the analgesia study and no immunosuppression, whereas a dose of 32.0 mg/kg produced a maximal analgesic effect and significant suppression of NK activity. Naltrexone blocked morphine-induced analgesia and immunosuppression in a dose-dependent fashion. Moreover, the combination of 1.0 mg/kg of naltrexone and 32.0 mg/kg of morphine elevated splenic NK activity. A large dose of morphine (100.0 mg/kg) elicited full analgesia and had no effect on splenic NK activity in saline- or naltrexone-pretreated mice. Collectively, these results support the view that, in mice, morphine-induced analgesia and immunosuppression are mediated through a common opioid receptor type.
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PMID:Naltrexone antagonizes the analgesic and immunosuppressive effects of morphine in mice. 818 37

Magnetic field exposure was consistently found to affect pain inhibition (i.e. analgesia). Recently, we showed that an extreme reduction of the ambient magnetic and electric environment, by mu-metal shielding, also affected stress-induced analgesia (SIA) in C57 mice. Using CD1 mice, we report here the same findings from replication studies performed independently in Pisa, Italy and London, ON, Canada. Also, neither selective vector nulling of the static component of the ambient magnetic field with Helmholtz coils, nor copper shielding of only the ambient electric field, affected SIA in mice. We further show that a pre-stress exposure to the mu-metal box is necessary for the anti-analgesic effects to occur. The differential effects of the two near-zero magnetic conditions may depend on the elimination (obtained only by mu-metal shielding) of the extremely weak time-varying component of the magnetic environment. This would provide the first direct and repeatable evidence for a behavioural and physiological effect of very weak time-varying magnetic fields, suggesting the existence of a very sensitive magnetic discrimination in the endogenous mechanisms that underlie SIA. This has important implications for other reported effects of exposures to very weak magnetic fields and for the theoretical work that considers the mechanisms underlying the biological detection of weak magnetic fields.
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PMID:Shielding, but not zeroing of the ambient magnetic field reduces stress-induced analgesia in mice. 1179 36

Mice that lack or over-express a gene of interest are important tools for unraveling gene function. The determination of single nephron function by micropuncture or precise determination of glomerular filtration rate (GFR) by inulin clearance method require experiments under anesthesia. A good anesthetic protocol should allow for reasonable and stable glomerular and tubular function. The aim of this study was to compare the commonly used thiobutabarbital (TBB) versus alpha-chloralose (CHL) anesthesia with regard to absolute levels and the stability of blood pressure, heart rate, and kidney function. Male CD1 mice were anesthetized with TBB (100 mg/kg body weight i.p.) or CHL (120 mg/kg body weight i.p.), plus ketamine (100 mg/kg body weight i.m.) given to every mouse for analgesia. After preparation for clearance experiments, two 30-min urine collections were performed at periods 1 and 2 (P1 and P2). It was observed that heart rate and mean arterial blood pressure did not differ between TBB ( n=9) vs. CHL ( n=9) and were stable through P1 and P2. In CHL, GFR as well as fractional excretion of fluid, Na(+) and K(+) were stable from P1 to P2 (P1: 190+/-15 microl/min, 1.6+/-0.2%, 0.7+/-0.1%, 35+/-5%; percent change in P2: 1+/-6, 26+/-10, 29+/-15, 6+/-10 respectively). In TBB, GFR was significantly greater vs. CHL in P1 and did not significantly change in P2 (246+/-8 microl/min, p<0.05; percent change: -6.5+/-4). Fractional excretion of fluid, Na(+) and K(+) were not significantly different vs. CHL in P1, but significantly increased in P2 (P1: 1.5+/-0.2%, 1.1+/-0.2%, 31+/-3%; percent change in P2: 122+/-23, 128+/-21 and 29+/-6 respectively; each p<0.05 vs. P1). In conclusion, mice under both anesthetic regimens present reasonable and stable blood pressure and reasonable kidney function, but kidney reabsorption is more stable under CHL than under TBB anesthesia, which may facilitate study of the response in kidney function to acute interventions.
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PMID:Kidney function in mice: thiobutabarbital versus alpha-chloralose anesthesia. 1554 74


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