In this issue, Wang and colleagues solve an important puzzle in the understanding of schizophrenia. Previous work has linked NMDA receptor hypofunction to schizophrenia and shown that individuals with schizophrenia have a suppressed steady-state cortical response to 40-Hz repetitive auditory stimulation. However, systemic application of NMDA antagonists paradoxically increases this cortical response in rodents. Here, by specifically applying NMDA receptor blockade in the auditory thalamus while measuring the acoustically-driven response in two cortical regions simultaneously, Wang and colleagues found the drop in the steady-state response that is seen in schizophrenia. These findings solve an important paradox in the field and suggest that specific thalamic neurochemical alterations may occur in the brain of individuals with schizophrenia. In addition, this work suggests that suppression of NMDA receptors in the thalamus may serve as a potential animal model for the disease.

中文翻译：

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正确的选择：听性丘脑中的NMDA受体可能是理解精神分裂症的关键。

在这个问题上，Wang和同事解决了对精神分裂症的理解中的一个重要难题。先前的工作已将NMDA受体功能低下与精神分裂症联系起来，并表明精神分裂症患者对40 Hz重复性听觉刺激的稳态皮质反应受到抑制。但是，NMDA拮抗剂的全身应用反常增加了啮齿动物的皮质反应。在这里，通过在听觉丘脑中专门应用NMDA受体阻滞剂，同时测量两个皮质区域的声驱动反应，Wang及其同事发现了精神分裂症中稳态反应的下降。这些发现解决了该领域的一个重要悖论，并表明特定的丘脑神经化学改变可能在精神分裂症患者的大脑中发生。