GLOBAL CEREBRAL-ISCHEMIA ASSOCIATED WITH CARDIAC-ARREST IN THE RAT .1. DYNAMICS OF EARLY NEURONAL CHANGES
GLOBAL CEREBRAL-ISCHEMIA ASSOCIATED WITH CARDIAC-ARREST IN THE RAT .1. DYNAMICS OF EARLY NEURONAL CHANGES
复制标题
DOI：
10.1038/jcbfm.1992.34
复制
发表时间：
1992-03-01
影响因子：
6.3
通讯作者：
KLATZO, I
中科院分区：
文献类型：
--
作者：
KAWAI, K;NITECKA, L;KLATZO, I
光镜神经元的变化进行了研究，在大鼠进行10分钟的全球缺血产生的主要心脏血管的压缩。 甲酚紫染色切片的观察结果显示，早期的变化主要涉及GABA能神经元在不同的位置。 在再循环15分钟后处死的大鼠中，这些变化的特征是出现清晰的外周区，并伴有剩余神经元细胞质的浓缩。 1小时后，这些区域似乎被分隔成单个珍珠状液泡，在丘脑网状核中尤其突出。 3 h后，胞浆空泡消失，神经元的变化，特别是在大脑皮质，纹状体，海马和黑质网状部，主要包括染色质增多或尼氏物质的损失。 2天后，大脑皮层和丘脑中偶尔含有具有明显大核仁的神经元。 7天后，海马显示CA1锥体神经元损失约50%，与放射层中强烈的小胶质细胞反应相关，而丘脑网状核中的神经元破坏更完全。 我们的观察结果表明，GABA能神经元的早期变化可能提供一个时期的神经元去抑制，从而有助于兴奋性缺血性损伤的GABA能电路连接的地区。
Light microscopic neuronal changes were studied in rats subjected to 10 min of global ischemia produced by compression of the major cardiac vessels. Observations of cresyl violet-stained sections revealed early changes involving predominantly GABAergic neurons in various locations. In rats killed 15 min after recirculation, the changes were characterized by the appearance of a clear peripheral zone with condensation of the remaining neuronal cytoplasm. After 1 h, these zones appeared to be compartmentalized into individual pearl-like vacuoles, especially prominent in the nucleus reticularis thalami. After 3 h, the cytoplasmic vacuoles disappeared and the neuronal changes, particularly in the cerebral cortex, striatum, hippocampus, and pars reticulata of the substantia nigra, consisted mainly of hyperchromasia or loss of Nissl substance. After 2 days, the cerebral cortex and thalamus contained occasional neurons with conspicuously large nucleoli. After 7 days, the hippocampus revealed an approximately 50% loss of CA1 pyramidal neurons, associated with intense microglial reactivity in the stratum radiatum, whereas the neuronal destruction was more complete in the nucleus reticularis thalami. Our observations suggest a possibility that early changes in GABAergic neurons may provide a period of neuronal disinhibition and thus contribute to an excitatory ischemic damage in regions connected by GABAergic circuitry.