Smith R E, Haroutunian V, Davis K L, Meador-Woodruff J H
Mental Health Research Institute and Department of Psychiatry, University of Michigan Medical School, 205 Zina Pitcher Place, Ann Arbor, MI 48109-0720, USA.
Neuroreport. 2001 Sep 17;12(13):2885-7. doi: 10.1097/00001756-200109170-00026.
Previously, we have reported alterations in thalamic NMDA receptor subunit and excitatory amino acid transporter expression in schizophrenia, consistent with the hypothesis that thalamic glutamatergic dysfunction may contribute to the pathophysiology of this illness. We have generalized this hypothesis to include other molecules of the glutamate synapse. Using riboprobes specific for human brain-specific Na+-dependent inorganic phosphate transporter (BNPi) and differentiation-associated Na+/Pi co-transporter (DNPi), both vesicular glutamate transporters, in situ hybridization was performed in the thalami of persons with schizophrenia and comparison subjects. We detected increased expression of DNPi mRNA in the thalamus in schizophrenia, while BNPi mRNA was not expressed in the thalamus in any subjects. These findings support the hypothesis of glutamatergic dysfunction in the thalamus in schizophrenia.
此前，我们报道过精神分裂症患者丘脑N-甲基-D-天冬氨酸（NMDA）受体亚基及兴奋性氨基酸转运体表达的改变，这与丘脑谷氨酸能功能障碍可能导致该疾病病理生理学改变的假说相符。我们已将这一假说推广至谷氨酸突触的其他分子。使用针对人脑特异性钠依赖性无机磷酸转运体（BNPi）和分化相关钠/磷酸共转运体（DNPi）（二者均为囊泡谷氨酸转运体）的核糖探针，对精神分裂症患者及对照受试者的丘脑进行原位杂交。我们检测到精神分裂症患者丘脑中DNPi mRNA表达增加，而在任何受试者的丘脑中均未检测到BNPi mRNA的表达。这些发现支持精神分裂症患者丘脑谷氨酸能功能障碍的假说。
