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mbined low doses of morphine (0.25 mg/kg) and thalidomide (5 mg/kg). Conversely, pretreatment with non-effective doses of either non-selective (L-NAME, 5 mg/kg, i.p.) or selective neuronal (7-nitroindazole, 30 mg/kg, i.p.) NO synthase (NOS) inhibitors significantly augmented the anticonvulsant effects of combined low doses of thalidomide and morphine, whereas the inducible NOS inhibitor aminoguanidine (100 mg/kg, i.p.) did not exert such effect. Our results indicate that opioidergic transmission and its interaction with neuronal NO sign

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