Knockout of p75NTR does not alter the viability of striatal neurons following a metabolic or excitotoxic injury

被引:2
|
作者
Hanbury, R
Chen, EY
Wuu, J
Kordower, JH
机构
[1] Rush Presbyterian St Lukes Med Ctr, Res Ctr Brain Repair, Chicago, IL 60612 USA
[2] Rush Presbyterian St Lukes Med Ctr, Dept Neurol Sci, Chicago, IL 60612 USA
[3] Rush Presbyterian St Lukes Med Ctr, Dept Neurol, Chicago, IL 60612 USA
关键词
p75(NTR); reactive astrocytes; neurodegeneration; knockout mice; striatum; DARPP-32; 3-NP; QA;
D O I
10.1385/JMN:20:2:93
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Following metabolic or excitotoxic injury to the striatum, there is de novo expression of the low-affinity p75 neurotrophin receptor (p75(NTR)). The novel expression of this pan neurotrophin receptor in rodents occurs within the lesion core and surrounding area, creating a division between viable and nonviable tissue. The present series of experiments sought to elucidate whether the p75(NTR) expression seen following metabolic and excitotoxic injury alters neuronal viability within the striatum. Toward this end, we compared the extent of striatal lesion created with quinolinic acid (QA) or 3-nitropropionic acid (3-NP) in p75(NTR) null and wild-type mice. Using stereological techniques, we found that the lesion volume and neuronal cell counts between p75(NTR) null and wild-type mice were similar 1, 2, and 4 weeks post-QA or -3-NP lesion. The results indicate that the expression of p75(NTR) within reactive astrocytes in the mouse striatum is not a key factor in protecting neuronal cell death following metabolic and excitotoxic insults.
引用
收藏
页码:93 / 102
页数:10
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