Spontaneous orofacial dyskinesias in a captive cynomolgus monkey: Implications for tardive dyskinesia
Identifieur interne : 006273 ( Main/Curation ); précédent : 006272; suivant : 006274Spontaneous orofacial dyskinesias in a captive cynomolgus monkey: Implications for tardive dyskinesia
Auteurs : Rupniak [Royaume-Uni] ; S. J. Tye [Royaume-Uni] ; M. J. Steventon [Royaume-Uni] ; S. Boyce [Royaume-Uni] ; S. D. Iversen [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1990.
English descriptors
- KwdEn :
- Acetylcholine, Animals, Benzazepines (pharmacology), Disease Models, Animal, Dopamine, Dose-Response Relationship, Drug, Dyskinesia, Dyskinesia, Drug-Induced (physiopathology), Facial Expression, Facial Muscles (physiopathology), Haloperidol (pharmacology), Institutionalization, Macaca fascicularis (physiology), Mastication (physiology), Movement Disorders (physiopathology), Physostigmine (pharmacology), Primates, Scopolamine Hydrobromide (pharmacology), Stereotyped Behavior (physiology).
- MESH :
- chemical , pharmacology : Benzazepines, Haloperidol, Physostigmine, Scopolamine Hydrobromide.
- physiology : Macaca fascicularis, Mastication, Stereotyped Behavior.
- physiopathology : Dyskinesia, Drug-Induced, Facial Muscles, Movement Disorders.
- Animals, Disease Models, Animal, Dose-Response Relationship, Drug, Facial Expression.
Abstract
We describe a syndrome of spontaneous orofacial dyskinesias and cage stereotypies in a singly housed adult cynomolgus monkey never previously exposed to neuroleptic drugs. Abnormal movements were readily suppressed by acute treatment with haloperidol (0.03–0.24 mg/kg i.m.) or SCH23390 (0.05–0.2 mg/kg i.m.) but not by physostigmine (0.005–0.04 mg/kg i.m.) or scopolamine (0.0025–0.04 mg/kg i.m.). The symptomatology and response to pharmacological manipulations was indistinguishable from that previously attributed to chronic neuroleptic treatment in primates. Our findings indicate that neuroleptic‐induced tardive dyskinesias in most primate studies have not been clearly demonstrated.
Url:
DOI: 10.1002/mds.870050410
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ISTEX:1A9CF1B2053B7A5B623CB3488B9A1216015F7B4CLe document en format XML
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<term>Dopamine</term>
<term>Dose-Response Relationship, Drug</term>
<term>Dyskinesia</term>
<term>Dyskinesia, Drug-Induced (physiopathology)</term>
<term>Facial Expression</term>
<term>Facial Muscles (physiopathology)</term>
<term>Haloperidol (pharmacology)</term>
<term>Institutionalization</term>
<term>Macaca fascicularis (physiology)</term>
<term>Mastication (physiology)</term>
<term>Movement Disorders (physiopathology)</term>
<term>Physostigmine (pharmacology)</term>
<term>Primates</term>
<term>Scopolamine Hydrobromide (pharmacology)</term>
<term>Stereotyped Behavior (physiology)</term>
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<term>Haloperidol</term>
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<term>Scopolamine Hydrobromide</term>
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<term>Disease Models, Animal</term>
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<front><div type="abstract" xml:lang="en">We describe a syndrome of spontaneous orofacial dyskinesias and cage stereotypies in a singly housed adult cynomolgus monkey never previously exposed to neuroleptic drugs. Abnormal movements were readily suppressed by acute treatment with haloperidol (0.03–0.24 mg/kg i.m.) or SCH23390 (0.05–0.2 mg/kg i.m.) but not by physostigmine (0.005–0.04 mg/kg i.m.) or scopolamine (0.0025–0.04 mg/kg i.m.). The symptomatology and response to pharmacological manipulations was indistinguishable from that previously attributed to chronic neuroleptic treatment in primates. Our findings indicate that neuroleptic‐induced tardive dyskinesias in most primate studies have not been clearly demonstrated.</div>
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