Oral tardive dyskinesia in the rat.
Oral tardive dyskinesia may develop due to neuroleptic therapy as a drug-induced disorder of the dopaminergic system of the brain. Long-term treatment with a neuroleptic drug impairing dopaminergic neurotransmission in the rat brain augments oral dyskinetic responses to dopaminergic agonists like apomorphine. In the present experiments, rats were pretreated daily with haloperidol for 3 weeks to cause a 'chronic' blockade in the striatal dopamine receptors. After a withdrawal period of 3 and 6 days, oral sensory stimulation was applied. On the following day the same groups were given apomorphine, and the oral stimulation was repeated. The rats pretreated daily with haloperidol had significantly higher dyskinesia scores than the rats pretreated with saline. The main observation with these sensitized rats was an increase in the frequency and intensity of experimental bruxism caused by oral sensory stimulation alone. Sensory impulses are known to cause release of dopamine in the nigrostriatal system. The combination of oral sensory stimulation and central dopaminergic supersensitivity in the rat can be regarded as an animal model for oral symptoms in human dyskinesia.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002012:Bruxism / Q000503:physiopathology*; D003769:Dental Occlusion, Traumatic / Q000503:physiopathology; D004195:Disease Models, Animal; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology*; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D013997:Time Factors
D011954:Receptors, Dopamine; D006220:Haloperidol; D001058:Apomorphine