Stoet Gijsbert, Snyder Lawrence H
Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, MO 63110, USA.
Neuropsychopharmacology. 2006 Aug;31(8):1675-81. doi: 10.1038/sj.npp.1300930. Epub 2005 Oct 5.
In humans, the effects of subanesthetic doses of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, substantially impair executive control functions. Here, we consider whether ketamine exposure can provide an animal model for the effects of ketamine on executive control. Two monkeys (Macaca mulatta) performed a cued task-switching paradigm. We studied their behavior before and after a range of ketamine doses. We found that ketamine slowed overall performance and decreased overall accuracy, strongly impaired the capacity to ignore task-irrelevant information and, to a lesser degree, decreased accuracy when a task switch was required. This pattern of results is very similar to that found in studies of schizophrenic patients performing task-switching paradigms or the Stroop task. We conclude that ketamine in monkeys provides a good animal model for exploring the relationship between the glutamate system, executive control, and the symptoms of schizophrenia.
在人类中，亚麻醉剂量的氯胺酮（一种N-甲基-D-天冬氨酸（NMDA）受体拮抗剂）会严重损害执行控制功能。在此，我们探讨氯胺酮暴露是否能为氯胺酮对执行控制的影响提供一个动物模型。两只猕猴（恒河猴）执行了一个线索任务切换范式。我们研究了它们在一系列氯胺酮剂量给药前后的行为。我们发现，氯胺酮减慢了整体表现并降低了整体准确性，严重损害了忽略任务无关信息的能力，并且在需要任务切换时，在较小程度上降低了准确性。这种结果模式与对执行任务切换范式或斯特鲁普任务的精神分裂症患者的研究结果非常相似。我们得出结论，猕猴中的氯胺酮为探索谷氨酸系统、执行控制和精神分裂症症状之间的关系提供了一个良好的动物模型。
