Changes in truncated trkB and p75 receptor expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment
Changes in truncated trkB and p75 receptor expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment
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DOI：
10.1006/exnr.2000.7480
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发表时间：
2000-10-01
影响因子：
5.3
通讯作者：
Priestley, JV
中科院分区：
文献类型：
--
作者：
King, VR;Bradbury, EJ;Priestley, JV
虽然许多研究已经检查了脊髓损伤后神经营养因子治疗的效果，但很少有研究检查了这种损伤或神经营养因子治疗后神经营养因子受体中发生的变化。为了确定脊髓损伤后神经营养因子受体表达发生了什么变化，成年大鼠单独或结合鞘内应用脑源性神经营养因子（BDNF）或神经营养因子-3（NT-3）接受了胸中段脊髓半切术。使用免疫组织化学和原位杂交技术，p75，trkA，trkB，和trkC受体的表达进行了检查整个脊髓。结果表明，trkA，全长trkB，和trkC受体不存在于损伤部位，但有一个正常的表达模式在脊髓未受伤的部分。相反，p75受体表达发生在整个病变部位的雪旺细胞上。BDNF和NT-3（但不是生理盐水）施加到病变部位增加这种表达。此外，截短的trkB受体表达在损伤和完整脊髓之间的边界。截断的trkB受体的表达也增加了整个白色物质同侧的病变和BDNF（但不是NT-3或盐水）防止这种增加。这项研究首次显示了截断的trkB受体表达的变化，这种变化超出了脊髓损伤的部位，并且是第一个显示BDNF和NT-3影响脊髓损伤后的雪旺细胞和/或p75表达的研究之一。这些结果表明，脊髓损伤后神经营养因子受体表达的变化可能会影响病变部位神经营养因子的可用性。此外，神经营养因子可能通过改变p75和截短的trkB受体的表达来影响其自身对受损神经元的可用性。(C)北京大学出版社.
Although numerous studies have examined the effects of neurotrophin treatment following spinal cord injury, few have examined the changes that occur in the neurotrophin receptors following either such damage or neurotrophin treatment. To determine what changes occur in neurotrophin receptor expression following spinal cord damage, adult rats received a midthoracic spinal cord hemisection alone or in combination with intrathecal application of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immunohistochemical and in situ hybridization techniques, p75, trkA trkB, and trkC receptor expression was examined throughout the spinal cord. Results showed that trkA, full-length trkB, and trkC receptors were not present in the lesion site but had a normal expression pattern ill uninjured parts of the spinal cord. In contrast, p75 receptor expression occurred on Schwann cells throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this expression. In addition, the truncated trkB receptor was expressed in the border between the lesion and intact spinal cord. Truncated trkB receptor expression was also increased throughout the white matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) prevented this increase. The study is the first to show changes in truncated trkB receptor expression that extend beyond the site of a spinal cord lesion and is one of the first to show that BDNF and NT-3 affect Schwann cells and/or p75 expression following spinal cord damage. These results indicate that changes in neurotrophin receptor expression following spinal cord injury could influence the availability of neurotrophins at the lesion site. In addition, neurotrophins may affect their own availability to damaged neurons by altering the expression of the p75 and truncated trkB receptor. (C) 2000 Academic Press.