Integrity of Cerebellar Fastigial Nucleus Intrinsic Neurons Is Critical for the Global Ischemic Preconditioning.
Integrity of Cerebellar Fastigial Nucleus Intrinsic Neurons Is Critical for the Global Ischemic Preconditioning.
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DOI：
10.3390/brainsci7100121
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发表时间：
2017-09-21
期刊：
影响因子：
3.3
通讯作者：
Britz GW
中科院分区：
文献类型：
--
作者：
Golanov EV;Regnier-Golanov AS;Britz GW
小脑顶核（FN）固有神经元的兴奋使大脑耐受局部和全局缺血。这种效果在刺激后72小时达到最大值，持续10天以上。类似的神经保护在亚致死性全脑缺血后被观察到，这种现象被称为预处理。我们假设FN可能作为内在神经保护机制的一部分参与了缺血预处理的机制。为了探讨FN神经元在脑缺血耐受中的潜在意义，我们在4-VO全脑缺血20 min前5天用兴奋毒素伊博tenic酸损伤内源性FN神经元，并在1周后分析海马角脑区1 （CA1）的神经元损伤情况。在fn损伤的动物中，CA1细胞的损失比对照组（注射磷酸盐缓冲盐水（PBS））动物高22%。此外，FN神经元损伤使全脑缺血后的发病率增加50%。消融FN神经元也逆转了5分钟缺血预处理对CA1神经元的挽救作用和发病率，而消融小脑齿状核神经元未改变缺血预处理的效果。我们认为FN是内在神经保护系统的重要组成部分，参与缺血预处理，并可能参与自然发生的神经保护，如“潜水反应”。
Excitation of intrinsic neurons of cerebellar fastigial nucleus (FN) renders brain tolerant to local and global ischemia. This effect reaches a maximum 72 h after the stimulation and lasts over 10 days. Comparable neuroprotection is observed following sublethal global brain ischemia, a phenomenon known as preconditioning. We hypothesized that FN may participate in the mechanisms of ischemic preconditioning as a part of the intrinsic neuroprotective mechanism. To explore potential significance of FN neurons in brain ischemic tolerance we lesioned intrinsic FN neurons with excitotoxin ibotenic acid five days before exposure to 20 min four-vessel occlusion (4-VO) global ischemia while analyzing neuronal damage in Cornu Ammoni area 1 (CA1) hippocampal area one week later. In FN-lesioned animals, loss of CA1 cells was higher by 22% compared to control (phosphate buffered saline (PBS)-injected) animals. Moreover, lesion of FN neurons increased morbidity following global ischemia by 50%. Ablation of FN neurons also reversed salvaging effects of five-minute ischemic preconditioning on CA1 neurons and morbidity, while ablation of cerebellar dentate nucleus neurons did not change effect of ischemic preconditioning. We conclude that FN is an important part of intrinsic neuroprotective system, which participates in ischemic preconditioning and may participate in naturally occurring neuroprotection, such as “diving response”.
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影响因子：
5.5
作者：
ACHARI, NK;DOWNMAN, CBB
通讯作者：
DOWNMAN, CBB
影响因子：
2.5
作者：
BRODAL, A;TABER, E;WALBERG, F
通讯作者：
WALBERG, F
DOI：
10.1016/0034-5687(70)90077-0
发表时间：
1970-01-01
期刊：
RESPIRATION PHYSIOLOGY
影响因子：
--
作者：
ELSNER, R;SHURLEY, JT;BROOKS, RE
通讯作者：
BROOKS, RE
影响因子：
2.4
作者：
Çavdar, S;San, T;Onat, F
通讯作者：
Onat, F
影响因子：
2.9
作者：
CHIDA, K;IADECOLA, C;REIS, DJ
通讯作者：
REIS, DJ