EXPERIMENTAL MODEL OF TARDIVE DYSKINESIA
EXPERIMENTAL MODEL OF TARDIVE DYSKINESIA
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DOI：
10.1007/bf01245320
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发表时间：
1972-01-01
影响因子：
3.3
通讯作者：
RUBOVITS, R
中科院分区：
文献类型：
--
作者：
KLAWANS, HL;RUBOVITS, R
胺诱导的刻板行为和迟发性运动障碍之间有许多临床和实验相似之处。这里的结果表明，慢性预处理的豚鼠与氯丙嗪产生持久的减少量的安非他明或阿朴吗啡需要诱导刻板行为。提示氯丙嗪预处理可改变纹状体多巴胺受体对多巴胺的敏感性。长时间氯丙嗪预处理产生的受体位点反应性的改变可能类似于精神抑制剂诱导的迟发性运动障碍。相同的多巴胺能机制可能是动物中所见的胺刻板行为和人类迟发性运动障碍的基础，而当纹状体中的多巴胺能反应增加时，舌面颊运动障碍可能是动物中所见的刻板行为的人类等价物。
There are numerous clinical and experimental similarities between amine induced stereotyped behavior and tardive dyskinesia. The results presented here show that chronic pretreatment of guinea pigs with chlorpromazine produces a persistent reduction in the amounts of amphetamine or apomorphine needed to induce stereotyped behavior. It is suggested that chlorpromazine pretreatment may alter the sensitivity of the striatal dopaminergic receptors to dopamine. The alteration in receptor site responsiveness produced by prolonged chlorpromazine pretreatment may be analogous to the neuroleptic induced tardive dyskinesias. The same dopaminergic mechanism may underlie both the amine stereotyped behavior seen in animals and tardive dyskinesias in man, while lingual-facial-buccal dyskinesias may be the human equivalent of the stereotypies seen in animals when the dopaminergic response in the striatum is increased.