Abstract：
A substantial body of evidence implicates dysfunction in N-methyl-d-aspartate receptors (NMDARs) in the pathophysiology of schizophrenia. This article illustrates how NMDAR dysfunction may give rise to many of the neurobiological phenomena frequently associated with schizophrenia with a particular focus on how NMDAR dysfunction affects the thalamic reticular nucleus (nRT) and pedunculopontine tegmental nucleus (PPTg). Furthermore, this article presents a model for schizophrenia illustrating how dysfunction in the nRT may interrupt prefrontal regulation of midbrain dopaminergic neurons, and how dysfunction in the PPTg may drive increased, irregular burst firing.
摘要：
大量证据表明精神分裂症的病理生理学中N-甲基-d-天冬氨酸受体（NMDARs）的功能障碍。本文说明了NMDAR功能障碍如何引起许多与精神分裂症经常相关的神经生物学现象，特别关注NMDAR功能障碍如何影响丘脑网状核（nRT）和足脑桥被盖核（PPTg）。此外，本文提出了一个精神分裂症模型，说明nRT中的功能障碍如何中断中脑多巴胺能神经元的前额叶调节，以及PPTg中的功能障碍如何驱动增加，不规则的爆发射击。
