Immunohistochemical localization of phosphorylated glial fibrillary acidic protein in the prefrontal cortex and hippocampus from patients with schizophrenia, bipolar disorder, and depression

被引:138
作者
Webster, MJ
Knable, MB
Johnston-Wilson, N
Nagata, K
Inagaki, M
Yolken, RH
机构
[1] Uniformed Serv Univ Hlth Sci, Stanley Lab Brain Res, Bethesda, MD 20814 USA
[2] Johns Hopkins Univ, Stanley Div Dev Neurovirol, Baltimore, MD 21287 USA
[3] Aichi Canc Ctr, Res Inst, Biochem Lab, Aichi 4640021, Japan
关键词
schizophrenia; major depression; bipolar disorder; neuropathology; glia;
D O I
10.1006/brbi.2001.0646
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Increasingly, abnormalities of glial cell function have been implicated in pathological studies of the major mental illnesses (schizophrenia, bipolar disorder, and major depression). In a recent proteomic study, four isoforms of astrocytic glial fibfillary acidic protein (GFAP) were decreased in one or more of these diseases. In the current study, we sought to determine the immunohistochemical localization of phosphorylated GFAP (pGFAP) in the prefrontal cortex and hippocampus and to describe possible disease-related changes in the distribution of pGFAP containing astrocytes. In the prefrontal cortex, interlaminar astrocytes in layer I and stellate astrocytes in layers II and VI were labeled. Labeled cells were also present adjacent to blood vessels in the gyral white matter and in underlying white matter generally. In the hippocampus. labeled cells were present in the polymorphic layer of the dentate gyrus. In the prefrontal cortex, schizophrenia and major depression were characterized by decreased labeling of astrocytes adjacent to blood vessels. There were no significant differences between the diagnostic groups in the other prefrontal layers or in the hippocampus. These results suggest that reduced numbers or functional regulation of pGFAP containing astrocytes occurs in schizophrenia and major depression. The mechanism by which this deficit occurs is not known, but it may adversely effect the regulation of neuronal metabolism, communication, and response to injury. (C) 2001 Elsevier Science.
引用
收藏
页码:388 / 400
页数:13
相关论文
共 45 条
[1]   Absence of neurodegeneration and neural injury in the cerebral cortex in a sample of elderly patients with schizophrenia [J].
Arnold, SE ;
Trojanowski, JQ ;
Gur, RE ;
Blackwell, P ;
Han, LY ;
Choi, C .
ARCHIVES OF GENERAL PSYCHIATRY, 1998, 55 (03) :225-232
[2]   Recent advances in defining the neuropathology of schizophrenia [J].
Arnold, SE ;
Trojanowski, JQ .
ACTA NEUROPATHOLOGICA, 1996, 92 (03) :217-231
[3]   IMPAIRMENT OF THE BLOOD-BRAIN-BARRIER AS AN ETIOLOGICAL FACTOR IN PARANOID PSYCHOSIS [J].
AXELSSON, R ;
MARTENSSON, E ;
ALLING, C .
BRITISH JOURNAL OF PSYCHIATRY, 1982, 141 (SEP) :273-281
[4]   BLOOD-CEREBROSPINAL FLUID BARRIER IN SCHIZOPHRENIC-PATIENTS [J].
BAUER, K ;
KORNHUBER, J .
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE, 1987, 236 (05) :257-259
[5]   Evidence for activation of microglia in patients with psychiatric illnesses [J].
Bayer, TA ;
Buslei, R ;
Havas, L ;
Falkai, P .
NEUROSCIENCE LETTERS, 1999, 271 (02) :126-128
[6]   PATTERNS OF GLIOSIS IN ALZHEIMERS-DISEASE AND AGING CEREBRUM [J].
BEACH, TG ;
WALKER, R ;
MCGEER, EG .
GLIA, 1989, 2 (06) :420-436
[7]  
BENES FM, 1986, ARCH GEN PSYCHIAT, V43, P31
[8]  
BENSHACHAR D, 1994, J NEUROCHEM, V62, P1112
[9]  
BERMAN KF, 1991, AM PSYCHIATRIC PRESS, V10, P24
[10]   HUMAN-IMMUNODEFICIENCY-VIRUS PROTEIN GP120 INTERFERES WITH BETA-ADRENERGIC RECEPTOR-MEDIATED PROTEIN-PHOSPHORYLATION IN CULTURED RAT CORTICAL ASTROCYTES [J].
BERNARDO, A ;
PATRIZIO, M ;
LEVI, G ;
PETRUCCI, TC .
CELLULAR AND MOLECULAR NEUROBIOLOGY, 1994, 14 (02) :159-173