Increased expression of growth-associated protein 43 on the surface of the anterior horn cells in amyotrophic lateral sclerosis

被引：0

作者：

A. Ikemoto

Asao Hirano

Ichiro Akiguchi

机构：

[1] Department of Neurology,

[2] Faculty of Medicine,undefined

[3] Kyoto University,undefined

[4] 54 Shogoin-Kawaharacho,undefined

[5] Sakyoku,undefined

[6] Kyoto 606,undefined

[7] Japan Tel.: +81-75-751-3766,undefined

[8] Fax: +81-75-751-3265,undefined

[9] Division of Neuropathology,undefined

[10] Department of Pathology,undefined

[11] Montefiore Medical Center,undefined

[12] 111 East 210th Street,undefined

[13] Bronx,undefined

[14] NY 10467,undefined

[15] USA,undefined

来源：

Acta Neuropathologica | 1999年 / 98卷

关键词：

Key words Amyotrophic lateral sclerosis; Anterior horn cell; Axonal terminal; Growth-associated protein 43; Synaptic plasticity;

D O I：

暂无

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学科分类号：

摘要：

This study examined axonal terminal alterations in the anterior horn of amyotrophic lateral sclerosis (ALS) patients. An antibody against growth-associated protein 43 (GAP43), a phosphoprotein which is expressed in elongating terminals of neurites, was employed for immunohistochemical staining. Lumbar spinal cords taken at autopsy from five ALS patients and from six control adults were examined. In control patients, there were numerous GAP43-positive granules diffusely dispersed throughout the anterior horn neuropil, and individual large anterior horn cells (AHCs) showed numerous tiny immunoreactive granules and small dots on the surface. A small number of AHCs showed dense accumulation of GAP43 immunoreactivity on the surface of the cell body and proximal processes. In all ALS patients, similar accumulation of GAP43 immunoreactivity was seen on the surface of a large number of remaining AHCs. Statistical analysis revealed a significant increase in number of AHCs with such accumulation in ALS patients. These results suggest that during the ALS disease process there may be plastic alterations or a compensatory mechanism of the axonal terminals located on the surface of some AHCs for ongoing anterior horn presynaptic terminal degeneration.

引用

页码：367 / 373

页数：6