RELATIVE LOSS OF THE STRIATAL STRIOSOME COMPARTMENT, DEFINED BY CALBINDIN-D(28K) IMMUNOSTAINING, FOLLOWING DEVELOPMENTAL HYPOXIC-ISCHEMIC I NJURY
RELATIVE LOSS OF THE STRIATAL STRIOSOME COMPARTMENT, DEFINED BY CALBINDIN-D(28K) IMMUNOSTAINING, FOLLOWING DEVELOPMENTAL HYPOXIC-ISCHEMIC I NJURY
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DOI：
10.1016/0306-4522(93)90333-b
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发表时间：
1993-09-01
期刊：
影响因子：
3.3
通讯作者：
BAIMBRIDGE, KG
中科院分区：
文献类型：
--
作者：
BURKE, RE;BAIMBRIDGE, KG
纹状体特别容易受到缺氧缺血性损伤，无论是在成年期还是在发育期间。纹状体损伤可能在发育性缺氧缺血导致的慢性运动控制异常中发挥重要作用。以前的研究表明，两个纹状体神经元表型，胆碱能和NADPH-黄递酶阳性，是耐发育性缺氧缺血，但很少有人知道其他纹状体神经元之间的脆弱性模式。特别是，没有关于主要纹状体神经元组（中型神经元）内脆弱性模式的数据。由于这些神经元的主要解剖和功能组织是在它们的本地化的纹状体或基质区室，我们已经检查了发育缺氧缺血对这些区室的影响，使用定量形态学分析的钙结合蛋白calbindin-D28 k的免疫染色。在总纹状体面积平均损失33%的情况下，纹状体面积减少49%。此外，纹状体的数量也减少了41%，单个纹状体的平均面积也有小幅（14%）但显著的减少。在吻尾向，纹状体的损失是均匀的。在细胞水平，钙结合蛋白阳性神经元的密度，表示为每单位面积的数量，被保存。虽然有几种可能的解释选择性损失的纹状体区室，一种假设是，这些神经元内的钙结合蛋白的水平较低，使他们更容易受到细胞内钙的增加，这已被假定在缺氧缺血性损伤中发挥作用。缺氧缺血性损伤后纹状体区室的主要损失可能导致功能不同的基质系统的失衡。这种不平衡可能导致这种形式的损伤后观察到的运动控制异常。
The striatum is especially vulnerable to hypoxic-ischemic injury, both in adulthood and during development. Striatal injury is likely to play a major role in the chronic abnormalities of motor control which occur as a consequence of developmental hypoxia-ischemia. Previous studies have shown that two striatal neuron phenotypes, cholinergic and NADPH-diaphorase-positive, are resistant to developmental hypoxia-ischemia, but little is otherwise known of patterns of vulnerability among other striatal neurons. In particular, there has been no data available about patterns of vulnerability within the major striatal neuron group, the medium-sized neurons. Since a major anatomical and functional organization of these neurons is in their localization to either the striosome or the matrix compartments, we have examined the effect of developmental hypoxia-ischemia on these compartments using a quantitative morphologic analysis of immunostaining for the calcium-binding protein calbindin-D28k.We have found that there is a predominant loss of the striosome compartment; in the presence of a mean loss of 33% of total striatal area, there was a 49% decrease in striosomal area. There was also a 41% reduction in the number of striosomes, and a small (14%) but significant decrease in the mean area of individual striosomes. The striosome loss was uniform in the rostrocaudal dimension. At a cellular level, the density of calbindin-positive neurons, expressed as number per unit area, was preserved. While there are several possible explanations for the selective loss of the striosome compartment, one hypothesis is that the lower level of calbindin within these neurons makes them more vulnerable to increases in intracellular calcium, which has been postulated to play a role in hypoxic-ischemic injury. The predominant loss of the striosome compartment following hypoxic ischemic injury may lead to an imbalance with the functionally distinct matrix system. Such an imbalance may contribute to the abnormalities of motor control observed after this form of injury.