Yurek D M, Randall P K
Life Sci. 1985 Nov 4;37(18):1665-73. doi: 10.1016/0024-3205(85)90293-0.
Intraventricular administration of haloperidol or chlorpromazine produces catalepsy and blocks apomorphine-induced stereotypic behavior. Low intraventricular doses of domperidone, sulpiride and spiperone, equally cataleptogenic as haloperidol or chlorpromazine, augment rather than diminish stereotypic behavior produced by subsequent apomorphine treatment. The resultant stereotypic behavior continues even while the animal is in a rigid cataleptic posture and is marked by persistent gnawing and licking. Prior to the induction of catalepsy and after recovery from it, mice display the entire range of typical apomorphine-induced behavior including sniffing, climbing, gnawing, and licking. This animal model may be related to the clinical observation of the coexistence of tardive dyskinesia and drug-induced Parkinsonism in individual patients.
脑室内注射氟哌啶醇或氯丙嗪会产生僵住症，并阻断阿扑吗啡诱导的刻板行为。脑室内注射低剂量的多潘立酮、舒必利和螺哌隆，其致僵住症作用与氟哌啶醇或氯丙嗪相当，反而会增强而非减弱后续阿扑吗啡治疗所产生的刻板行为。即使动物处于僵硬的僵住症姿势时，由此产生的刻板行为仍会持续，其特征为持续的啃咬和舔舐。在僵住症诱发之前及从僵住症恢复之后，小鼠会表现出阿扑吗啡诱导的一系列典型行为，包括嗅探、攀爬、啃咬和舔舐。该动物模型可能与个体患者中迟发性运动障碍和药物性帕金森病共存的临床观察结果相关。
