The temporal evolution of neuronal damage from pilocarpine-induced status epilepticus
The temporal evolution of neuronal damage from pilocarpine-induced status epilepticus
复制标题
DOI：
10.1016/0006-8993(96)00203-x
复制
发表时间：
1996-06-24
期刊：
影响因子：
2.9
通讯作者：
Fujikawa, DG
中科院分区：
文献类型：
--
作者：
Fujikawa, DG
用光镜观察了匹罗卡品致痫后不可逆神经元损伤的时间演变。通过估计23个脑区嗜酸性神经元的百分比来判断神经细胞死亡的程度，评分为0-3。此外，在背齿状门(CA4)，还进行了正常神经元和嗜酸性神经元的定量细胞计数。癫痫持续状态(SE)20min后，腹侧海马CA1、CA3区出现少量死亡神经元(0.5级损伤)。40min和I-h SE分别有14个和12个脑区出现轻中度损伤(0.5~1.5级)，3h SE后15个区出现轻中度损伤(0.5~2.0级)。3h SE后24 h和72 h，分别有22个和21个区域出现轻至重度损伤(0.5~3.0级)。与I-h SE相比，3h SE对7个脑区的损伤更严重，其中16个区域的神经元损伤在24 h后较3 h后0~4 h明显加重，8个脑区在SE后72 h较24 h损伤较轻，可能是由于神经元的逐渐溶解和脱落所致，但SE后24~72 h，背内侧和丘脑后外侧核团的损伤加重。神经元细胞计数显示，癫痫发作40min后齿状核嗜酸性神经元占20%，而L惊厥3h组和癫痫发作3h组之间无明显差异(分别为31%和43%)。在3h SE和不同恢复期的3组大鼠中，恢复24 h和72 h组的嗜酸性神经元百分比(分别为65%和54%)高于0-4 h组(43%)。最后，被认为对癫痫诱导的细胞损伤具有抵抗力的海马CA2区和齿状颗粒细胞层以及尾壳核均受到持续40min或更长时间的SE的损害。
The temporal evolution of irreversible neuronal damage from pilocarpine-induced seizures was studied by light microscopy. Neuronal cell death was judged on a 0-3 scale by estimating the percentage of acidophilic neurons in each of 23 brain regions. In addition, in the dorsal dentate hilus (CA4), quantitative cell counts of normal and acidophilic neurons were also performed. A few dead neurons (grade 0.5 damage) appeared in ventral hippocampal CA1 and CA3 regions after 20-min status epilepticus (SE). Slight-to-mild damage (grades 0.5-1.5) occurred in 14 and 12 brain regions after 40-min and I-h SE respectively, and slight-to-moderate damage (grades 0.5-2.0) was found in 15 regions after 3-h SE. Twenty-four h and 72 h after 3-h SE, there was slight-to-severe damage (grade 0.5-3.0) in 22 and 21 regions respectively. Three-h SE produced more severe damage to 7 brain regions compared to I-h SE, and 16 regions had more pronounced neuronal injury 24 h after rather than 0-4 h after 3-h SE, Eight brain regions had less damage 72 h compared to 24 h after SE, probably because of progressive neuronal lysis and dropout, but in mediodorsal and lateroposterior thalamic nuclei damage worsened from 24 to 72 h after SE. Neuronal cell counting revealed 20% acidophilic neurons in dorsal dentate hilus after 40-min SE and no difference between the l-h and 3-h seizure groups (31% vs. 43% acidophilic neurons respectively). Among the 3 groups of rats with 3-h SE and varying recovery periods, the 24-h and 72-h recovery groups had higher percentages of acidophilic neurons (65% and 54% respectively) than the 0-4-h group (43%). Finally, the hippocampal CA2 region and dentate granule cell layer and the caudate-putamen, considered resistant to seizure-induced cell injury, were all damaged from SE lasting 40 min or more.