Response to Morphine in a unicellular animal model (Paramecium caudatum)

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Introduction: Response to morphine and role of Nitric Oxide (NO) on expression of morphine response has been studied in vertebrates. But, little evidence is provided in the matter in earlier invertebrates. This investigation for the first time evaluated the effect of NO on expression of morphine potency in Paramecium caudatum. Methods: Animal after isolation from natural media and specific identification was cultured in laboratory. 1 ml of the isolated medium including the animals was added into the Sedgwick– Rafter cell counter. One μl of drugs was infused into the cell counter. Morphine (1-60 μg/μl) was infused into the cell and its effect was recorded throughout 0- 180 sec. L-Arginine (1-8 μg/μl), a NO precursor, was infused prior to morphine (2 μg/μl). The NO producing enzyme was inhibited by preinfusion of L-NAME. Also the naloxone was used to show the involvement of the opioid receptors in the signaling of morphine response. In control speciements distilled water was added solely. Results: The Paramecia under the infusion of morphine were aggregated. The most aggregation rate was observed at a relatively low dose of the drug (2 μg/μl). L-Arginine showed a positive effect on the response (p<0.001) whearas the effect was blocked by preinfusion of the L- NAME. Naloxone showed an inhibitory effect to morphine response. The activity of the NOS was shown by using the NADPH-diaphorase. Conclusion: A sign of morphine potency in single–celled animal is the cell aggregation, and the present results are showing the interaction of NO system with the opioidergic system in this line. On the other hand, concerning the potentiation effect of L-arginine on morphine effective dose in the model, this finding may be useful in reducing of morphine’s side effects in patients under the treatment of the drug, and in the drug economy as well.

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response to morphine in a unicellular animal model (paramecium caudatum)

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عنوان ژورنال

دوره 15  شماره None

صفحات  318- 329

تاریخ انتشار 2011-10

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