Pharmacological mitigation of tissue damage during brain microdialysis.
Pharmacological mitigation of tissue damage during brain microdialysis.
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DOI：
10.1021/ac401201x
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发表时间：
2013-09-03
影响因子：
7.4
通讯作者：
Michael, Adrian C.
中科院分区：
文献类型：
--
作者：
Nesbitt, Kathryn M.;Jaquins-Gerstl, Andrea;Skoda, Erin M.;Wipf, Peter;Michael, Adrian C.
脑微透析取样常用于神经功能和疾病的化学分析。但是，植入比脑细胞和血管的大小和间距大得多的探针是有害的，会在采样部位引发缺血、胶质细胞增生和细胞死亡。大脑和微透析探针之间界面的性质对于使用微透析作为神经化学分析技术至关重要。本研究的目的是研究两种化合物地塞米松（糖皮质激素抗炎剂）和XJB-5-131（线粒体靶向活性氧清除剂）减轻穿透损伤的潜力。测量是在大鼠大脑纹状体中进行的，纹状体密集地由释放多巴胺的轴突支配，多巴胺是一种电活性神经递质。我们使用伏安法测量地塞米松或XJB-5-131后透析过程中微透析探针旁的电诱发多巴胺释放。在体内测量后，用荧光显微镜检查含有微透析探针轨迹的脑组织，使用缺血、神经元核、巨噬细胞、多巴胺轴突和终末标记。地塞米松和XJB-5-131均能减轻诱发多巴胺活性的丧失，减轻缺血，减轻神经元核的丧失，减轻外渗巨噬细胞的外观，减轻探针旁多巴胺轴突和终末的丧失。我们的研究结果证实了地塞米松和XJB-5-131能够减轻，但不能消除植入微透析探针引起的脑组织穿透损伤的影响。
Microdialysis sampling in the brain is employed frequently in the chemical analysis of neurological function and disease. But, implanting the probes, which are substantially larger than the size and spacing of brain cells and blood vessels, is injurious and triggers ischemia, gliosis, and cell death at the sampling site. The nature of the interface between the brain and the microdialysis probe is critical to the use of microdialysis as a neurochemical analysis technique. The objective of the work reported here was to investigate the potential of two compounds, dexamethasone, a glucocorticoid anti-inflammatory agent, and XJB-5-131, a mitochondrially-targeted reactive oxygen species scavenger, to mitigate the penetration injury. Measurements were performed in the rat brain striatum, which is densely innervated by axons that release dopamine, an electroactive neurotransmitter. We used voltammetry to measure electrically evoked dopamine release next to microdialysis probes during the retrodialysis of dexamethasone or XJB-5-131. After the in vivo measurements, the brain tissue containing the microdialysis probe tracks was examined by fluorescence microscopy using markers for ischemia, neuronal nuclei, macrophages, and dopamine axons and terminals. Dexamethasone and XJB-5-131 each diminished the loss of evoked dopamine activity, diminished ischemia, diminished the loss of neuronal nuclei, diminished the appearance of extravasated macrophages, and diminished the loss of dopamine axons and terminals next to the probes. Our findings confirm the ability of dexamethasone and XJB-5-131 to mitigate, but not eliminate, the effects of the penetration injury caused by implanting microdialysis probes into brain tissue.
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影响因子：
7.4
作者：
Jaquins-Gerstl, Andrea;Shu, Zhan;Zhang, Jing;Liu, Yansheng;Weber, Stephen G.;Michael, Adrian C.
通讯作者：
Michael, Adrian C.
影响因子：
12.7
作者：
BENVENISTE, H;DIEMER, NH
通讯作者：
DIEMER, NH
影响因子：
3
作者：
Borland, LM;Shi, GY;Michael, AC
通讯作者：
Michael, AC
影响因子：
14
作者：
Karumbaiah, Lohitash;Norman, Sharon E.;Bellamkonda, Ravi V.
通讯作者：
Bellamkonda, Ravi V.
影响因子：
9.7
作者：
Hsiao, Tony W.;Swarup, Vimal P.;Kuberan, Balagurunathan;Tresco, Patrick A.;Hlady, Vladimir
通讯作者：
Hlady, Vladimir