Abnormal glycosylation of EAAT1 and EAAT2 in prefrontal cortex of elderly patients with schizophrenia

SCHIZOPHRENIA RESEARCH

卷:117

Article

Bauer, Deborah^1,2  Haroutunian, Vahram³  Meador-Woodruff, James H.^1,2  McCullumsmith, Robert E.¹ 

[1] Univ Alabama, Dept Psychiat & Behav Neurobiol, Birmingham, AL 35294 USA

[2] Univ Michigan, Neurosci Program, Ann Arbor, MI 48109 USA

[3] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA

关键词: GLAST;    GLT-1;    EAAC1;    Deglycosylation;    Anterior cingulate cortex;    Dorsolateral prefrontal cortex;   

DOI  :  10.1016/j.schres.2009.07.025

来源: Elsevier

【 摘 要 】

The excitatory amino acid transporters (EAATs) are a family of molecules that are essential for regulation of synaptic glutamate levels. The EAATs may also be regulated by N-glycosylation, a post translational modification that is critical for many cellular functions including localization in the plasma membrane. We hypothesized that glycosylation of the EAATs is abnormal in schizophrenia. To test this hypothesis, we treated postmortem tissue from the dorsolateral prefrontal and anterior cingulate cortices of patients with schizophrenia and comparison Subjects with deglycosylating enzymes. We then measured the resulting shifts in molecular weight of the EAATs using Western blot analysis to determine the mass of glycans cleaved from the transporter. We found evidence for less glycosylation of both EAAT1 and EAAT2 in schizophrenia. We did not detect N-linked glycosylation of EAAT3 in either schizophrenia or the comparison subjects in these regions. Our data Suggest an abnormality of posttranslational modification of glutamate transporters in schizophrenia that Suggests a decreased capacity for glutamate reuptake. Published by Elsevier B.V.

【 授权许可】

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