Immunohistochemical study of brain-derived neurotrophic factor and its receptor, TrkB, in the hippocampal formation of schizophrenic brains

被引:84
|
作者
Iritani, S
Niizato, K
Nawa, H
Ikeda, K
Emson, PC
机构
[1] Tokyo Metropolitan Matsuzawa Hosp, Dept Psychiat, Tokyo 1560057, Japan
[2] Niigata Univ, Brain Res Inst, Dept Mol Biol, Niigata, Japan
[3] Tokyo Inst Psychiat, Dept Neuropathol, Tokyo, Japan
[4] Babraham Inst, Dept Neurobiol, Cambridge, England
来源
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY | 2003年 / 27卷 / 05期
关键词
BDNF; hippocampus; immunohistochemistry; TrkB;
D O I
10.1016/S0278-5846(03)00112-X
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Recently, the pathogenesis of schizophrenia has been investigated from the perspective of neurodevelopmental dysfunction theory. On the other hand, it has been indicated that neurotrophic factors, such as nerve growth factors, brain-derived neurotrophic factor (BDNF), and neurotrophin-3, are significantly involved in the development and functional differences of central nervous system (CNS). Some reports proposed that the dysfunction of these factors could explain the pathogenesis of schizophrenia possibly. In this study, the authors investigated immumohistochemically the distribution and/or morphology of BDNF and TrkB, its peculiar receptor, in the hippocampal formation of schizophrenic brain. As a result, BDNF-positive pyramidal cells in the CA2 and neurons in the CA3 and the field of the CA4 were intensely stained compared to those of normal control. Staining of TrkB-positive neurons showed a signet-ring like shape in the hippocampus of normal control brains. Such figures were not observed on staining of those neurons from schizophrenic brains. In the control cases, TrkB-immunopositive varicose fibers were frequently seen. Those observed differences between schizophrenic and normal cases may indicate the existence of dysfunction of BDNF and TrkB in schizophrenic brain, and this dysfunction may be one of the factors involved in the pathogenesis of schizophrenia. (C) 2003 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:801 / 807
页数:7
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