Morphine, an analgesic with significant abuse potential, is considered addictive because of drug craving and psychological dependence. It is reported that repeated treatment of morphine can produce conditioned place preference (CPP) showing a reinforcing effect in mice. CPP is a useful method for th...
Morphine, an analgesic with significant abuse potential, is considered addictive because of drug craving and psychological dependence. It is reported that repeated treatment of morphine can produce conditioned place preference (CPP) showing a reinforcing effect in mice. CPP is a useful method for the screening of morphine-induced psychological dependence. In the present study, we investigated the effect of the methanolic extract of Coptis japonica (MCJ) on morphine-induced CPP in mice. Furthermore, we examined c-fos expression in the parietal cortex, piriform cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. Treatment of MCJ 100 mg/kg inhibited morphine-induced CPP. Expression of c-fos was increased in the cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. These increases of expression were inhibited by treatment with MCJ 100 mg/kg, compared to the morphine control group. Taken together, these results suggest that MCJ inhibits morphine-induced CPP through the regulation of c-fos expression in the mouse brain.
Morphine, an analgesic with significant abuse potential, is considered addictive because of drug craving and psychological dependence. It is reported that repeated treatment of morphine can produce conditioned place preference (CPP) showing a reinforcing effect in mice. CPP is a useful method for the screening of morphine-induced psychological dependence. In the present study, we investigated the effect of the methanolic extract of Coptis japonica (MCJ) on morphine-induced CPP in mice. Furthermore, we examined c-fos expression in the parietal cortex, piriform cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. Treatment of MCJ 100 mg/kg inhibited morphine-induced CPP. Expression of c-fos was increased in the cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. These increases of expression were inhibited by treatment with MCJ 100 mg/kg, compared to the morphine control group. Taken together, these results suggest that MCJ inhibits morphine-induced CPP through the regulation of c-fos expression in the mouse brain.
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대상 데이터
M기, ? ICR mice (MJ Ltd., Seoul, Korea) weehing 18-24 g at tie beginning of the experiment were used. They were housed 10 mice to a cage with water and food availaole ad libitum under an artificial 12 h light/dark cy이e (light at 7 :00 a.
, Seoul, Korea) weehing 18-24 g at tie beginning of the experiment were used. They were housed 10 mice to a cage with water and food availaole ad libitum under an artificial 12 h light/dark cy이e (light at 7 :00 a.m.) and constant temperature (22t2℃).
데이터처리
The data were expressed as mean±S.E.M. Statistical analysis was carried out by one-way analysis of variance (ANOVA). In the case of significant variation, the individual values were compared by the St니de가 Newman-Keuls test.
이론/모형
Statistical analysis was carried out by one-way analysis of variance (ANOVA). In the case of significant variation, the individual values were compared by the St니de가 Newman-Keuls test. The criterion for significance was p<0.
후속연구
These results suggest that MCJ could inhibit morphino-induced CPP via modulation of the dopaminergic system. Therefore, further studies are needed to elucidate the in /olcement of dopaminergic systems in the inhibitory effect of MCJ on morphine-induced CPP.
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