Kurumaji A, Wakai T, Toru M
Department of Neuropsychiatry, Tokyo Medical and Dental University School of Medicine, Japan.
J Neural Transm (Vienna). 1997;104(11-12):1361-70. doi: 10.1007/BF01294737.
We measured the peripheral-type benzodiazepine receptors (PBRs), a marker of gliosis, in 26 brain areas (cerebral cortex, thalamus and extrapyramidal system) of the postmortem brains of 13 chronic schizophrenics and 10 controls, using [3H] PK 11195 as a ligand for the receptor assay. The specific [3H] PK 11195 binding was significantly decreased in three brain areas (superior parietal cortex, primary visual area and putamen) of schizophrenics, although there were no changes in the binding in the other brain areas. Scatchard analysis revealed that there were decreases in both the Bmax and Kd of [3H] PK 11195 binding in the brain areas. These results were almost in accordance with a number of neuropathological studies reporting that there was no change or reduction in glial cells in the brain regions of schizophrenics and suggested that the decreased density of PBRs in the brain may be involved in the pathophysiology of schizophrenia, associated with reduced production of neurosteroids coupled to PBRs.
我们使用[3H] PK 11195作为受体测定的配体,对13名慢性精神分裂症患者和10名对照者的死后大脑的26个脑区(大脑皮层、丘脑和锥体外系)中的外周型苯二氮䓬受体(PBRs)进行了测量,PBRs是胶质细胞增生的标志物。精神分裂症患者的三个脑区(顶上叶皮层、初级视觉区和壳核)中,[3H] PK 11195的特异性结合显著降低,尽管其他脑区的结合没有变化。Scatchard分析显示,这些脑区中[3H] PK 11195结合的Bmax和Kd均降低。这些结果几乎与一些神经病理学研究一致,这些研究报告称精神分裂症患者脑区的胶质细胞没有变化或减少,这表明大脑中PBRs密度降低可能参与了精神分裂症的病理生理学过程,与与PBRs相关的神经甾体生成减少有关。