Plasticity of aged perivascular axons following exogenous NGF: analysis of catecholamines.
Plasticity of aged perivascular axons following exogenous NGF: analysis of catecholamines.
复制标题
外源性 NGF 后老化血管周围轴突的可塑性：儿茶酚胺分析。
DOI：
10.1016/s0197-4580(01)00238-x
复制
发表时间：
2002
影响因子：
4.2
通讯作者：
Isaacson,LG
中科院分区：
文献类型：
--
作者：
Dickason,AK;Isaacson,LG
本研究探讨了老年人血管周围交感神经轴突的萎缩和这些脑血管神经元对神经营养因子神经生长因子（NGF）的反应。采用高效液相色谱-电化学检测（HPLC-ECD）定量儿茶酚胺和免疫组织化学方法定量TH免疫反应纤维的密度，我们发现，去甲肾上腺素（NE）和TH在老年交感神经轴突显着减少。然而，在体内施用外源性神经营养因子后，老年神经元对NGF表现出与年轻成人相似的强烈反应，这表明老年神经元利用外源性神经营养因子的能力几乎没有下降。这些结果表明，老年交感神经轴突与年龄相关的萎缩可能主要是由于靶源性神经营养因子的可用性减少而不是神经元功能的内在改变造成的。
The present study investigated the atrophy of aged perivascular sympathetic axons and the response of these cerebrovascular neurons to the neurotrophin nerve growth factor (NGF). Using high performance liquid chromatography coupled with electrochemical detection (HPLC-ECD) to quantify catecholamines and immunohistochemical methods to quantify the density of TH immunoreactive fibers, we found a significant decrease in norepinephrine (NE) and TH in aged sympathetic axons. However, following in vivo administration of exogenous neurotrophin, aged neurons exhibited a robust response to NGF that was similar to the young adult, suggesting little decline in the capability of aged neurons to utilize exogenous neurotrophin. These results suggest that the age-related atrophy of aged sympathetic axons may result primarily from reduced availability of target-derived neurotrophin rather than from intrinsic alterations of neuronal function.