Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this experiment is to investigate genetic differences in the development of physical dependence on morphine and codeine in inbred strains of mice, C57BL/6, C3H/He and DBA/2. Mice were treated with morphine- or codeine-admixed food (1, 2 and 3 mg/g of food) for 3 to 9 days. After the termination of drug treatment, the mice were given naloxone (5 mg/kg, s.c.). The incidences of jumping and teeth chattering by naloxone challenge in morphine- and codeine-treated C57BL/6 mice were much greater than those in C3H/He and DBA/2 mice. However, the incidences of other naloxone-precipitated withdrawal signs, such as ptosis and diarrhea, were not different among the three inbred strains of mice. These results indicate that genotype is an important determinant of the degree of most naloxone-precipitated withdrawal signs in morphine- and codeine-treated mice.
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PMID:Differential sensitivity to physical dependence on morphine and codeine in three inbred strains of mice. 180 63

The anticonvulsant action of various aporphine derivatives that act on dopamine receptors has been investigated in two genetically determined animal models--DBA/2 mice with sound-induced seizures and baboons Papio papio with photically-induced seizures. Protection against the clonic and tonic phases of the seizures response in DBA/2 mice was seen for 15-60 min after (-)2,10,11-trihydroxy-N-n-propylnoraporphine (1.25 mg/kg) and (-)10,11-methyl-enedioxy-N-n-propylnoraporphine (0.625-1.25 mg/kg) and for 30-60 min after (-)2,10,11-trihydroxyaporphine (31.25 mg/kg). Short-lasting protection (up to 30 min) was seen following (-)2,10,11-trihydroxy-N-ethyl-noraporphine (1.25-6.25 mg/kg). Changes in audiogenic seizure susceptibility were accompanied by piloerection, ptosis and loss of spontaneous locomotor and exploratory behaviour. No protection was seen after (-)norapomorphine (0.05-18.75 mg/kg). All the compounds (including norapomorphine) significantly lowered rectal temperature, although the time course of this effect was often longer than that of protection against audiogenic seizures. In baboons, marked reductions in photomyoclonic responses were seen following (-)10,11-methylenedioxy-N-n-propylnoraporphine (0.25 mg/kg, lasting up to 2h); (-)2,10,11-trihydroxy-N-n-propylnoraporphine (0.5-2.5 mg/kg, lasting up to 7 h); (-)2,10,11-trihydroxyaporphine (5 mg/kg, duration of action 1-4 h) and (-)2,10,11-trihydroxy-N-ethylnoraporphine (6.25 mg/kg, lasting 2 h). Little change in responsiveness followed administration of (-)norapomorphine 1.25 or 6.25 mg/kg. Changes in photosensitivity were accompanied by yawning and pupil dilatation. (-)10,11-Methylenedioxy-N-n-propylnoraporphine (0.5-6.25 mg/kg) was also administered orally in baboons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative assessment of dopamine agonist aporphines as anticonvulsants in two models of reflex epilepsy. 641 43

Audiogenic seizures associated with loss of weight, prostration, piloerection, palpebral ptosis and motor deficiency were induced after sound stimulation of determined frequency and amplitude in magnesium-deficient DBA/2 mice. These symptoms were maintained when standard diet conditions (1700 ppm Mg2+) were restored. In contrast, mice were protected from audiogenic seizure in a dose related manner when Crassostrea gigas extract (JCOE) were added to the diet for 10 consecutive days. Although a rational explanation for this protective effect has not yet been determined, it is assumed that it might be due to a chelating complex formed between Mg2+ and taurine, which enhance the uptake of Mg2+.
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PMID:Protective effect of Crassostrea gigas extract on audiogenic seizures in magnesium deficient mice. 975 10