Nialamide-induced hypermotility in mice treated with inhibitors of monoamine uptake, 5-HT antagonists and lithium.

When administered orally to mice 1 h before nialamide 100 mg/kg SC two non-selective and nine selective 5-HT uptake inhibitors enhanced the hypermotility produced by nialamide, whereas two inhibitors of NA uptake showed no influence on the nialamide response. Paroxetine was the most potent nialamide potentiator; 100% increase in motility response was obtained at 0.012 mg/kg. Pretreatment with the 5-HT2 antagonist ritanserin 1 and 10 mg/kg SC reduced the hypermotility produced by nialamide 200 mg/kg SC, but the 5-HT1 antagonist L-propranolol 10 mg/kg administered similarly was found inactive. Nialamide 100 mg/kg was given SC to groups of mice being treated for 4 weeks with paroxetine and lithium given through the diet. At daily intakes of paroxetine and lithium resulting in therapeutic plasma or serum levels a distinctive nialamide potentiation was found.