Abnormal expression of glutamate transporter and transporter interacting molecules in prefrontal cortex in elderly patients with schizophrenia

被引:80
作者
Bauer, Deborah [1 ,2 ]
Gupta, Daya [3 ]
Harotunian, Vabram [4 ]
Meador-Woodruff, James H. [1 ,2 ]
McCullumsmith, Robert E. [1 ]
机构
[1] Univ Alabama Birmingham, Dept Psychiat & Behav Neurobiol, Birmingham, AL 35294 USA
[2] Univ Michigan, Neurosci Program, Ann Arbor, MI 48109 USA
[3] SUNY, Dept Biochem, New York, NY USA
[4] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA
关键词
GPS1; anterior cingulate cortex; dorsolateral prefrontal cortex; postmortem; Western blot; in situ hybridization;
D O I
10.1016/j.schres.2008.06.012
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Glutamate cycling is critically important for neurotransmission, and may be altered in schizophrenia. The excitatory amino acid transporters (EAATs) facilitate the reuptake of glutamate from the synaptic cleft and have a key role in glutamate cycling. We hypothesized that expression of the EAATs and the EAAT regulating proteins ARHGEF11, JWA, G-protein suppressor pathway I (GPSI), and KIAA0302 are altered in the brain ill schizophrenia. To test this, we measured express ion of EAAT1, EAAT2, EAAT3, and EAAT interacting proteins in postmortem tissue from the dorsolateral prefrontal and anterior cingulate cortex of patients with schizophrenia and a comparison group using in situ hybridization and Western blot analysis. We found increased EAAT I transcripts and decreased protein expression, increased EAAT3 transcripts and protein, and elevated protein expression of both GPSI and KIAA0302 protein. We did not find any changes in expression of EAAT2. These data indicate that proteins involved in glutamate reuptake and cycling are altered in the cortex ill schizophrenia, and may provide potential targets for future treatment strategies. Published by Elsevier B.V.
引用
收藏
页码:108 / 120
页数:13
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