مشخصات پژوهش

صفحه نخست /Nicotine restores ...
عنوان Nicotine restores morphine-induced memory deficit through the D1 and D2 dopamine receptor mechanisms in the nucleus accumbens
نوع پژوهش مقاله چاپ‌شده در مجلات علمی
کلیدواژه‌ها Morphine - Nicotine - SCH23390 - Sulpiride - Retrieval - Rat
چکیده Involvement of the dopamine D1 and D2 receptors in the nucleus accumbens (NAc) in interaction between morphine and nicotine on inhibitory avoidance (IA) memory was investigated. A step-through type of inhibitory avoidance tasks was used to assess memory in male Wistar rats. The results showed that subcutaneous (s.c.) administration of morphine (7.5 mg/kg) after training decreased retrieval of IA memory in the animals when tested 24 h later. Pre-test administration of the same dose of morphine significantly reversed the deficiency in retrieval. The results also showed that pre-test administration of nicotine (0.2 and 0.4 mg/kg, s.c.) by itself mimicked the effect of pre-test morphine, and lower doses of nicotine (0.1 and 0.2 mg/kg) also improved the effect of a low dose of morphine (2.5 mg/kg) on retrieval of IA memory. Pre-test intra-NAc administration of the dopamine D1 receptor antagonist, SCH23390 (0.001 and 0.01 µg/rat), and the dopamine D2 receptor antagonist, sulpiride (0.5 and 1 µg/rat) caused no significant effects on IA memory by themselves, but both prevented reinstatement of the retrieval of IA memory by the effective dose of nicotine (0.4 mg/kg). It can be concluded that the dopaminergic mechanism(s) in the NAc is a cross-link for the effect of morphine and nicotine on reinstatement of retrieval of IA memory impaired by post-training administration of morphine.
پژوهشگران شمس الدین احمدی (نفر دوم)، وهاب باباپور (نفر سوم)، آمنه رضایوف (نفر چهارم)، محمد رضا زرین دست (نفر پنجم)، روناک عزیزبیگی (نفر اول)