Ohnuma T, Kato H, Arai H, Faull R L, McKenna P J, Emson P C
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Neuroreport. 2000 Sep 28;11(14):3133-7. doi: 10.1097/00001756-200009280-00019.
A number of studies have suggested that disturbance in glutamatergic transmission in the cerebral cortex may underlie, or contribute to the pathophysiology of schizophrenia. In this study we examined expression of the postsynaptic density protein 95 (PSD95) mRNA in the prefrontal cortex and hippocampus in postmortem material from neuroleptic-treated schizophrenics and normal controls. PSD95 is known to bind to NMDA receptor subunits and is known to be involved in synaptic plasticity. In situ hybridization analysis showed that the expression of PSD95 was significantly decreased in Brodmann area 9 of the prefrontal cortex but not in the hippocampus. These results further implicate the prefrontal cortex in the pathophysiology of schizophrenia and suggest dysfunction of NMDA receptors in the schizophrenic cortex.
多项研究表明，大脑皮层谷氨酸能传递紊乱可能是精神分裂症病理生理学的基础或促成因素。在本研究中，我们检测了经抗精神病药物治疗的精神分裂症患者和正常对照者死后脑组织中前额叶皮质和海马体中突触后致密蛋白95（PSD95）mRNA的表达。已知PSD95可与NMDA受体亚基结合，并参与突触可塑性。原位杂交分析显示，前额叶皮质Brodmann 9区中PSD95的表达显著降低，但海马体中未降低。这些结果进一步表明前额叶皮质与精神分裂症的病理生理学有关，并提示精神分裂症患者皮质中NMDA受体功能异常。
