Sumiyoshi T, Ichikawa J, Meltzer H Y
Department of Psychiatry, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA.
Pharmacol Biochem Behav. 1997 May-Jun;57(1-2):19-22. doi: 10.1016/s0091-3057(96)00126-8.
The incidence of S(-)-apomorphine-induced vacuous chewing movements (VCMs) as a model for tardive dyskinesia was investigated in streptozotocin (STZ)-induced diabetic rats. A single dose of STZ (65 mg/kg, intravenously) caused a diabetic state (hyperglycemia, 480-490 vs. 116-118 mg/dl in naive rats). S(-)-apomorphine (250 micrograms/kg, subcutaneously)-induced VCMs were significantly intensified in diabetic rats which had received STZ 9 weeks previously. The enhancement of VCMs was also observed in nondiabetic rats which received subsequent treatment with depot haloperidol (4 mg/kg, intramuscularly, once a week, every week for 4 weeks) followed by a 2-week washout period. The ability of haloperidol to enhance VCMs was attenuated in diabetic rats. The implications of these results in relation to altered neurotransmissions in STZ-induced diabetes are discussed.
以S(-)-阿扑吗啡诱导的空嚼运动（VCMs）作为迟发性运动障碍模型，在链脲佐菌素（STZ）诱导的糖尿病大鼠中研究了其发生率。单次静脉注射STZ（65 mg/kg）导致糖尿病状态（血糖升高，480 - 490 vs. 未处理大鼠的116 - 118 mg/dl）。9周前接受过STZ的糖尿病大鼠中，皮下注射S(-)-阿扑吗啡（250微克/千克）诱导的VCMs显著增强。在接受长效氟哌啶醇（4 mg/kg，肌肉注射，每周一次，共4周）后续治疗并经过2周洗脱期的非糖尿病大鼠中也观察到VCMs增强。氟哌啶醇增强VCMs的能力在糖尿病大鼠中减弱。讨论了这些结果与STZ诱导糖尿病中神经传递改变的关系。
