Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Schizophr Bull. 2012 Sep;38(5):950-7. doi: 10.1093/schbul/sbs010. Epub 2012 Feb 21.
Gamma oscillations appear to be dependent on inhibitory neurotransmission from parvalbumin (PV)-containing gamma-amino butyric acid neurons. Thus, the abnormalities in PV neurons found in schizophrenia may underlie the deficits of gamma-band synchrony in the illness. Because gamma-band synchrony is thought to be crucial for cognition, cognitive deficits in schizophrenia may reflect PV neuron dysfunction in cortical neural circuits. Interestingly, it has been suggested that PV alterations in schizophrenia are the consequence of a hypofunction of signaling through N-methyl-D-aspartate (NMDA) receptors (NMDARs). Here, we review recent findings that address the question of how NMDAR hypofunction might produce deficits of PV neuron-mediated inhibition in schizophrenia. We conclude that while dysregulation of NMDARs may play an important role in the pathophysiology of schizophrenia, additional research is required to determine the particular cell type(s) that mediate dysfunctional NMDAR signaling in the illness.
伽马振荡似乎依赖于含有小白蛋白（PV）的γ-氨基丁酸神经元的抑制性神经传递。因此，在精神分裂症中发现的 PV 神经元异常可能是该疾病中伽马频带同步性缺陷的基础。由于伽马频带同步性被认为对认知至关重要，因此精神分裂症的认知缺陷可能反映了皮质神经回路中 PV 神经元功能障碍。有趣的是，有人提出精神分裂症中的 PV 改变是 N-甲基-D-天冬氨酸（NMDA）受体（NMDAR）信号转导功能低下的结果。在这里，我们回顾了最近的研究结果，这些结果解决了 NMDA 受体功能低下如何导致精神分裂症中 PV 神经元介导的抑制作用缺陷的问题。我们的结论是，尽管 NMDA 受体的失调可能在精神分裂症的病理生理学中发挥重要作用，但需要进一步的研究来确定在该疾病中介导功能障碍 NMDA 信号转导的特定细胞类型。
