Stoessl A J, Dourish C T, Iversen S D
Merck Sharp & Dohme Research Laboratories, Harlow, Essex, UK.
Psychopharmacology (Berl). 1987;93(3):336-42. doi: 10.1007/BF00187253.
Apomorphine-induced yawning was studied in male rats with bilateral 6-hydroxydopamine lesions of the substantia nigra. Apomorphine 10, 20 and 50 micrograms/kg SC induced dose-dependent yawning in unoperated controls and animals with sham lesions. In the lesioned animals (in which the mean striatal dopamine depletion was 67%), the maximum yawning response rate was greatly attenuated with no evidence that the dose response curve was shifted in either direction. Furthermore, blockade of yawning in the lesioned animals was not simply due to suppression by other stereotyped behaviours, since there was no evidence of increased sniffing or chewing in these animals. These data provide further support for the hypothesis that apomorphine-induced yawning is mediated by dopamine autoreceptors and requires intact nigrostriatal projections.
对患有双侧黑质6-羟基多巴胺损伤的雄性大鼠进行了阿扑吗啡诱导打哈欠的研究。阿扑吗啡10、20和50微克/千克皮下注射,在未手术的对照组和假损伤动物中诱导出剂量依赖性打哈欠。在损伤动物中(平均纹状体多巴胺耗竭率为67%),最大打哈欠反应率大大减弱,没有证据表明剂量反应曲线向任何一个方向移动。此外,损伤动物中打哈欠的阻断并非仅仅是由于其他刻板行为的抑制,因为没有证据表明这些动物的嗅闻或咀嚼增加。这些数据为阿扑吗啡诱导打哈欠由多巴胺自身受体介导且需要完整的黑质纹状体投射这一假说提供了进一步支持。