Ischemia-induced disturbance of neuronal network function in the rat spinal cord analyzed by voltage-imaging
Ischemia-induced disturbance of neuronal network function in the rat spinal cord analyzed by voltage-imaging
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DOI：
10.1016/j.neuroscience.2006.03.034
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发表时间：
2006-01-01
期刊：
影响因子：
3.3
通讯作者：
Toyama, Y.
中科院分区：
文献类型：
--
作者：
Fukuda, K.;Okada, Y.;Toyama, Y.
采用电压显像技术，分析了缺血、缺氧和低血糖对大鼠脊髓神经网络功能的急性影响。缺血、缺氧或低血糖应激分别用无氧和无葡萄糖、无氧或无葡萄糖的模拟脑脊液加载到脊髓切片中。背根刺激引起的背角去极化信号由快（突触前）和慢（突触后）组成。在缺血状态下，慢速组分比快速组分衰减更大（P < 0.0002）。III-IV层突触后神经元活性比I-II层更早受到抑制。神经纤维对缺血有较强的抵抗力。只要在背角中保留快成分，对快成分和慢成分的抑制是可逆的。快组分受缺血抑制20%以上组与慢组分受缺血抑制20%以下组恢复的慢组分大小差异有统计学意义（P < 0.05）。进一步延长应力不可逆地消除了大部分慢速成分，并减弱了快速成分（至59 +/- 8%），并伴有组织学上的细胞损伤。低氧或低血糖应激对神经活动的抑制不如缺血明显。长时间缺血应激可突然不可逆地消除腹角去极化信号，并伴有运动神经元的形态损伤。免疫组化染色未见细胞凋亡。我们首次通过直接观察脊髓内区域神经网络的活动，在神经网络水平上分析了缺血、缺氧、低血糖引起脊髓紊乱的过程。我们的结论是，背角的突触传递，特别是在深层区域，是脆弱的，并首先受到这些压力的影响。严重的缺血应激诱导神经元不可逆功能障碍，并最终导致背角和腹角细胞死亡。(c) 2006 IBRO。Elsevier Ltd.出版。版权所有。
Using a voltage-imaging technique, we analyzed the acute effect of ischemia, hypoxia and hypoglycemia on the neuronal network function of the rat spinal cord. Ischemic, hypoxic, or hypoglycemic stress was loaded to spinal cord slices with an oxygen- and glucose-free, oxygen-free, or glucose-free mock cerebrospinal fluid, respectively. Depolarizing signals in the dorsal horn, induced by dorsal root stimulation, consisted of fast (pre-synaptic) and slow (post-synaptic) components. The slow component was attenuated much more than the fast component under an ischemic condition (P < 0.0002). Post-synaptic neuronal activities in lamina III-IV were suppressed earlier than those in lamina I-II. The nerve fiber was relatively resistant to ischemia. As long as the fast component was preserved in the dorsal horn, the suppression of the fast and slow components was reversible. There was a significant difference (P < 0.05) in the recovered slow component sizes between the group in which the fast component was suppressed by more than 20% by ischemia and the group in which the suppression was less than 20%. Further prolonged stress irreversibly eliminated most of the slow component, and attenuated the fast component (to 59 +/- 8%) accompanied by cellular damage in histology. Suppression of neural activity by hypoxic or hypoglycemic stress was less prominent than that by ischemia. Prolonged ischemic stress suddenly and irreversibly eliminated depolarizing signals in the ventral horn accompanied by morphological damage of motoneurons. Immunohistochemical staining was negative for apoptosis. We have, for the first time, analyzed the processes of spinal cord disturbance induced by ischemia, hypoxia and hypoglycemia at the neuronal network level by directly observing the regional neuronal network activities within the spinal cord. We conclude that synaptic transmission in the dorsal horn, especially in deep regions, is vulnerable and first affected by these stresses. Severe ischemic stress induces irreversible dysfunction of neurons accompanied by eventual cell death in both dorsal and ventral horns. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.