Spreading depolarizations mediate excitotoxicity in the development of acute cortical lesions.
作者： Jason M. Hinzman , Vince A. DiNapoli , Eric J. Mahoney , Greg A. Gerhardt , Jed A. Hartings
DOI: 10.1016/J.EXPNEUROL.2015.03.014
关键词:
摘要: Abstract Spreading depolarizations (SD) are mass of neurons and astrocytes that occur spontaneously in acute brain injury mediate time-dependent lesion growth. Glutamate excitotoxicity has also been extensively studied as a mechanism neuronal injury, although its relevance to vivo pathology remains unclear. Here we hypothesized development occurs only consequence SD. Using glutamate-sensitive microelectrodes, found SD induced by KCl normal rat cortex elicits increases extracellular glutamate (11.6 ± 1.3 μM) synchronous with the onset, sustainment, resolution direct-current shift Inhibition uptake d , l -threo-β-benzyloxyaspartate (TBOA, 0.5 1 mM) significantly prolonged duration (148% 426%, respectively) increase (167% 374%, dose-dependent manner (P
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