• Takatoshi Sorimachi, Hiroshi Abe, Shigekazu Takeuchi, and Ryuichi Tanaka.
• Department of Neurosurgery, Brain Research Institute, Niigata University, Japan. sorimachi-t@h2.dion.ne.jp
• J. Neurosurg. 2002 Jul 1;97(1):104-11.

ObjectThe authors investigate whether depolarization monitoring is an accurate index of ischemic damage in a gerbil model of unilateral ischemia and assess the effects of brief cerebral ischemia on protein synthesis in this model.MethodsThe authors evaluate the relationship between the duration of ischemic depolarization caused by unilateral carotid artery occlusion and ischemia-induced neuronal damage in the CA1 subregion 7 days after ischemia. When the depolarization period exceeded 210 seconds, some neuronal damage was detected, and almost complete neuronal damage was observed when the period exceeded 400 seconds. Uptake of [14C]valine was evaluated in ischemic and nonischemic CA1 subregions. Disturbances in protein synthesis were seen in all animals subjected to sublethal ischemia (< or = 210-second depolarization) after a 10-minute recirculation, and after 2 and 6 hours of recirculation in animals with 90 seconds or more of depolarization. Inhibition of protein synthesis was proportional to the length of the depolarization period. After 1 and 3 days of recirculation, protein synthesis returned to near normal, and some animals with depolarizations greater than 180 to 210 seconds showed an increase in protein synthesis. Protein synthesis in all animals returned to normal levels after 7 days of recirculation.ConclusionsIn this study the authors demonstrate that monitoring of ischemic depolarization is a useful method to predict neuronal damage in the hippocampal CA1 in this model, and they identify subtle changes in protein synthesis after brief ischemia. Sublethal ischemia was divided into three categories by its depolarization period (< 90 seconds, 90-180 seconds, and > 180-210 seconds) with regard to changes in protein synthesis.

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