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)

The choline analog, N-amino-N,N-dimethylaminoethanol (NADe), was fed ad libitum (chloride salt; 0.5%) to weanling rats in a low choline, low methionine synthetic diet. Control rats were fed choline chloride (0.5%) in place of NADe. Initial observation and behavioral screen tests of grasp strength, startle reflex, righting reflex, analgesia (hot plate test) and body temperature did not reveal any toxic effects caused by NADe, although both experimental and control groups gained weight more slowly than rats fed standard lab chow. After 25 days on the diet, the performance of rats fed NADe in a one-trial passive avoidance test was significantly impaired compared to control rats. There was no difference between experimental and control rats in sensitivity to foot shock or in activity monitored in a closed field. A subjective, 6-component behavioral rating scale indicated rats fed NADe were resistant to handling but not aggressive. These behavioral results were similar in two separate feeding experiments using deuterium-labeled and unlabeled NADe. The twitch response of isolated rat phrenic nerve-diaphragms during stimulation did not show any impairment of neuromuscular function in rats fed NADe. Receptor binding experiments indicated there were no differences between experimental and control rats in tritiated quinuclidinyl benzilate [( 3H]QNB) binding capacity in cortex, heart and ileum. Competitive [3H]QNB binding with carbachol indicated there was no difference in the IC50's measured in cortex homogenates. Acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities in cortex were similar in experimental and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of chronic dietary administration of the cholinergic false precursor N-amino-N,N-dimethylaminoethanol on behavior and cholinergic parameters in rats. 301 61

Chronic morphine treatment (subcutaneous pellet implantation of four morphine pellets) caused significant tolerance to morphine analgesia as observed at zero and 6 hrs. after pellet removal. However, such treatment failed to elicit any changes in striatal muscarinic receptors using (3H)-QNB binding studies. At 24 hours after pellet removal there was significant development of physical dependence but the affinity (Kd) as well as density (Bmax) of striatal muscarinic receptors remained unaffected. Although naloxone caused marked precipitation of abrupt withdrawal in morphine tolerant rats, it also failed to produce any changes in striatal muscarinic receptors. Results indicate that any cholinergic involvement in opiate tolerance and physical dependence does not involve an effect on muscarinic receptors.
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PMID:The binding of 3H-quinuclidinyl benzilate to cholinergic muscarinic receptors in rat brain region following chronic treatment with morphine and during abstinence. 654 85

The antiarrhythmic drug tocainide (5a) and some related chiral alpha-amino and alpha-imino anilides (5b-e) were synthesized in optically active form. The antinociceptive effects of the different stereoisomers of these compounds were examined and it was found that the analgesic effect of tocainide is due only to its (-)-(R)-enantiomer. Benzyl replacement for methyl group at the stereogenic centre of tocainide causes loss of activity while both enantiomers of the alpha-iminoxilidide 5e and of the strictly related tocainide analog 5d produce an analgesic effect without any stereoselectivity. Pharmacological tests and [3H] quinuclidinyl benzilate ([3H]QNB) binding assay, taken together, seem to show that the antinociceptive effect of (-)-(R)-tocainide, like the analgesia induced by lidocaine, procaine, and mexiletine, is due to a central presynaptic cholinergic mechanism of action.
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PMID:Stereoselectivity in central analgesic action of tocainide and its analogs. 833 23