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.
Buus Lassen
J
J
Research Division, A/S Ferrosan, Soeborg, Denmark.
D000818:Animals; D004032:Diet; D005260:Female; D008094:Lithium / Q000097:blood / Q000494:pharmacology*; D051379:Mice; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology*; D009043:Motor Activity / Q000187:drug effects*; D009526:Nialamide / Q000494:pharmacology*; D017374:Paroxetine; D010880:Piperidines / Q000097:blood; D012702:Serotonin Antagonists / Q000494:pharmacology*
D008996:Monoamine Oxidase Inhibitors; D010880:Piperidines; D012702:Serotonin Antagonists; D017374:Paroxetine; D008094:Lithium; D009526:Nialamide