Rupniak N M, Jenner P, Marsden C D
Psychopharmacology (Berl). 1985;85(1):71-9. doi: 10.1007/BF00427326.
Continuous administration of haloperidol, sulpiride, or cis-flupenthixol, but not of domperidone or apomorphine, to Wistar rats for up to 3 weeks caused an increase in spontaneous purposeless chewing movements. Treatment with physostigmine and pilocarpine, but not neostigmine, for up to 3 weeks increased chewing, whilst scopolamine decreased chewing. Metergoline and cyproheptadine, but not quipazine, increased chewing after only 1 and 7 days but not thereafter. Chewing was not altered following treatment with compounds acting on GABA or noradrenaline systems or by a range of non-neuroleptic agents inducing dystonia in man. The enhancement of chewing induced by neuroleptic and cholinomimetic drugs was reduced by acute treatment with scopolamine, and reverted to control levels following drug withdrawal. Neuroleptic-induced purposeless chewing in Wistar rats appears to be primarily influenced by cerebral dopamine and acetylcholine function and may resemble acute dystonia, rather than tardive dyskinesia.
对Wistar大鼠连续3周给予氟哌啶醇、舒必利或顺式氟奋乃静，但不给予多潘立酮或阿扑吗啡，会导致自发性无目的咀嚼运动增加。连续3周用毒扁豆碱和毛果芸香碱治疗，但不用新斯的明，会增加咀嚼，而东莨菪碱则会减少咀嚼。美替拉酮和赛庚啶仅在1天和7天后增加咀嚼，之后则不再增加。用作用于GABA或去甲肾上腺素系统的化合物或一系列在人类中诱发肌张力障碍的非抗精神病药物治疗后，咀嚼没有改变。东莨菪碱急性治疗可降低抗精神病药物和拟胆碱药物诱导的咀嚼增强，停药后恢复到对照水平。Wistar大鼠中抗精神病药物诱导的无目的咀嚼似乎主要受脑多巴胺和乙酰胆碱功能影响，可能类似于急性肌张力障碍，而非迟发性运动障碍。
