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  • 1
    Electronic Resource
    Electronic Resource
    Oral dyskinesia in rats following brain lesions and neuroleptic drug administration (1982)
    Springer
    Psychopharmacology 77 (1982), S. 134-139 
    Details
    ISSN: 1432-2072
    Keywords: Animal model ; Rat ; Tardive dyskinesia ; Oral dyskinesia ; Chronic haloperidol ; Neuroleptic ; 6-Hydroxydopamine ; Kainic acid ; Frontal cortex ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract After 10–12 weeks of chronic haloperidol administration rats with frontal cortex ablations or lesions induced by intracerebroventricular injection of 6-hydroxydopamine developed vacuous chewing behavior at a fairly stable frequency (bifrontal ablations had 15–20, 6-hydroxy-dopamine lesioned rats 7–12 chewing movements/min). This behavior persisted for 10 weeks after the last injection of haloperidol decanoate. However, rats with frontal cortex lesions developed a low rate of vacuous chewings (4–8 chewings/min) even without haloperidol administration. Bilateral intrastriatal injections of kainic acid in combination with chronic haloperidol administration did not cause chewing movements in excess of unlesioned haloperidol-treated controls. Pharmacological tests of this animal model for tardive dyskinesia (TD) revealed similarities to human TD, but also differences. Dopamine agonists (apomorphine) and antagonists (haloperidol) both lowered chewing behavior analogous to reported effects on TD and so did gabaculine. The cholinergic drugs physostigmine and pilocarpine, however, increased chewing in rats, while anticholinergics (atropine) reduced it, in contrast to reported effects on human TD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00431935
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Haloperidol-induced tardive dyskinesia in monkeys (1976)
    Springer
    Psychopharmacology 50 (1976), S. 237-240 
    Details
    ISSN: 1432-2072
    Keywords: Tardive dyskinesia ; Acute dystonia ; Haloperidol ; Animal model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In three cebus monkeys the chronic daily administration of haloperidol (0.5 mg/kg/day orally) created sedation and parkinsonism during the first 5–7 weeks. Later the animals developed signs reminiscent of acute dystonia, as seen in the clinic during treatment with neuroleptics. These signs were dose-dependent and in extreme cases included widespread tonic and clonic seizures. After 3 and 12 months, respectively, two of the cebus monkeys developed buccolingual signs (grimacing and tongue protrusion), similar to tardive dyskinesia in the clinic. The tardive dyskinesia symptoms were reduced in a dose-dependent manner after each haloperidol administration, being most pronounced in the morning before haloperidol was given. Biperiden reduced acute dystonia but reinstated signs of tardive dyskinesia, which had been abolished by haloperidol. It is suggested that cebus monkeys may provide a useful animal model for the study of neurologic long-term complications from neuroleptic drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00426838
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    A monitoring test for the liability of neuroleptic drugs to induce tardive dyskinesia (1979)
    Springer
    Psychopharmacology 63 (1979), S. 195-198 
    Details
    ISSN: 1432-2072
    Keywords: Tardive dyskinesia ; Animal model ; Rebound deterioration sign ; Monitoring neurological side effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two Cebus apella monkeys with haloperidol-induced tardive dyskinesia have been studied. Substitution of chlorpromazine, thioridazine, clozapine, melperone, or fluphenazine for the daily haloperidol administration temporarily reduced the signs of tardive dyskinesia. In a monkey with low-grade symptoms, persisting for more than 100 days after with-drawal of haloperidol, neuroleptic drugs induced a typical sequence of events: first the dyskinetic movements were abolished, but 1–3 days after administration of a single dose of a neuroleptic drug there was a rebound worsening of symptoms. It was noticed that this aggravation of symptoms corresponded in magnitude and duration to the approximate liability of each compound to induce tardive dyskinesia in man. It is therefore suggested that this animal model could be used to monitor neurological side effects in neuroleptic drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00433548
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    Paper (German National Licenses)
    Fulltext
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