Differential spread of anoxic depolarization contributes to the pattern of neuronal injury after oxygen and glucose deprivation (OGD) in the Substantia Nigra in rat brain slices

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• 作者：Rashika N. Karunasinghe ; Angus C. Grey ; Ravindra Telang ; Srdjan M. Vlajkovic ; Janusz Lipski ; ^{j.lipski@auckland.ac.nz}
• 关键词：9AA ; 9-aminoacridine ; ACSF ; artificial cerebrospinal fluid ; AD ; anoxic depolarization ; CMFDA ; 5-chloromethylfluoroscein diacetate ; DA ; dopamine ; DPCPX ; dipropylcyclopentylxanthine ; EC ; energy charge ; LT ; light transmittance ; MALDI MS ; matrix assisted laser desorption/ionization mass spectrometry ; MAP2 ; microtubule associated protein 2 ; OGD ; oxygen glucose deprivation ; Rm ; cell input resistance ; SD ; spreading depression ; SN ; Substantia Nigra ; SNc ; Substantia Nigra pars compacta ; SNr ; Substantia N
• 刊名：Neuroscience
• 出版年：2017
• 出版时间：6 January 2017
• 年：2017
• 卷：340
• 期：Complete
• 页码：359-372
• 全文大小：3713 K
• 卷排序：340

文摘

Oxygen-glucose deprivation (OGD) mimicks many features of brain ischemia. OGD evokes differential responses in the Substantia Nigra in brain slice. During OGD, anoxic depolarization (AD) occurred only in the SN pars reticulata (SNr). The absence of AD in the SN pars compacta (SNc) reflects resilience of its dopaminergic neurons. The differing ischemic responses may explain the mechanisms underlying acute-onset motor disorders.