Costa Ana Luísa Lamounier, Silva Ronaldo Coelho, Coelho-Cordeiro Pedro H, da Silveira Fernando Silva, Barros Marilia, Caixeta Fabio Viegas, Maior Rafael S
Primate Center, Institute of Biology, University of Brasília, Brasilia, Brazil.
Laboratory of Neuroscience and Behavior, Department of Physiological Sciences, Institute of Biological Sciences, University of Brasília, Brasilia, Brazil.
Front Behav Neurosci. 2021 May 28;15:641776. doi: 10.3389/fnbeh.2021.641776. eCollection 2021.
The Müller-Lyer Illusion (MLI) has been suggested as a potential marker for the perceptual impairments observed in schizophrenia patients. Along with some positive symptoms, these deficits are not easily modeled in rodent experiments, and novel animal models are warranted. Previously, MK-801 was shown to reduce susceptibility to MLI in monkeys, raising the prospects of an effective perception-based model. Here, we evaluate the translational feasibility of the MLI task under NMDA receptor blockage as a primate model for schizophrenia. In Experiment 1, eight capuchin monkeys ( spp.) were trained on a touchscreen MLI task. Upon reaching the learning criteria, the monkeys were given ketamine (0.3 mg/kg; i.m.) or saline on four consecutive days and then retested on the MLI task. In Experiment 2, eight chronic schizophrenia patients (and eight matching controls) were tested on the Brentano version of the MLI. Under saline treatment, monkeys were susceptible to MLI, similarly to healthy human participants. Repeated ketamine administrations, however, failed to improve their performance as previous results with MK-801 had shown. Schizophrenic patients, on the other hand, showed a higher susceptibility to MLI when compared to healthy controls. In light of the present and previous studies, the MLI task shows consistent results across monkeys and humans. In spite of potentially being an interesting translational model of schizophrenia, the MLI task warrants further refinement in non-human primates and a broader sample of schizophrenia subtypes.
米勒-莱尔错觉(MLI)已被认为是精神分裂症患者所观察到的感知障碍的一个潜在标志物。除了一些阳性症状外,这些缺陷在啮齿动物实验中不容易建模,因此需要新的动物模型。此前,已证明MK-801可降低猴子对MLI的易感性,这为建立一个基于感知的有效模型带来了希望。在此,我们评估在NMDA受体阻断下MLI任务作为精神分裂症灵长类动物模型的转化可行性。在实验1中,八只卷尾猴(僧帽猴属)接受了触摸屏MLI任务训练。达到学习标准后,连续四天给猴子注射氯胺酮(0.3毫克/千克;肌肉注射)或生理盐水,然后对其进行MLI任务重新测试。在实验2中,八名慢性精神分裂症患者(以及八名匹配的对照组)接受了布伦塔诺版MLI测试。在生理盐水治疗下,猴子对MLI敏感,这与健康人类参与者类似。然而,与之前MK-801的结果不同,重复注射氯胺酮未能改善它们的表现。另一方面,与健康对照组相比,精神分裂症患者对MLI表现出更高的易感性。根据目前和之前的研究,MLI任务在猴子和人类中显示出一致的结果。尽管MLI任务可能是一个有趣的精神分裂症转化模型,但它仍需要在非人类灵长类动物中进一步完善,并纳入更广泛的精神分裂症亚型样本。