The mitochondrial toxin 3-nitropropionic acid induces vacuous chewing movements in rats. Implications for tardive dyskinesia?
Rats were chronically treated for 4 weeks with three doses (4, 8, 12 mg/kg per day) of the mitochondrial toxin 3-nitropropionic acid (3-NP). The behaviour was videotaped at intervals during and after treatment, and vacuous chewing movements (VCM), a putative analogue to tardive dyskinesia (TD), as well as the general behaviour were scored. During treatment, 3-NP dose-dependently increased VCM and dose-dependently reduced motor activity, which is similar to the behavioural effect of long-term neuroleptic treatment. The results may support the hypothesis that neuroleptic-induced impairment of energy metabolism, a potential excitotoxic mechanism, is involved in the development of VCM in rats and probably TD in humans.
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D004409:Dyskinesia, Drug-Induced; D005260:Female; D008409:Mastication / Q000187:drug effects*; D008928:Mitochondria / Q000187:drug effects; D009068:Movement / Q000187:drug effects*; D009498:Neurotoxins / Q000494:pharmacology*; D009574:Nitro Compounds; D011422:Propionates / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D009498:Neurotoxins; D009574:Nitro Compounds; D011422:Propionates; C015392:3-nitropropionic acid