CALCIUM MOVEMENT IN ISCHEMIA-TOLERANT HIPPOCAMPAL CA1 NEURONS AFTER TRANSIENT FOREBRAIN ISCHEMIA IN GERBILS

Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ische mia, acquired tolerance to a subsequent lethal 5-min period of ischemi a, which usually causes delayed-type neuronal death. Intracelluar Ca2 movements before and after the 5 min of forebrain ischemia were evalu ated in gerbil hippocampal CA1 pyramidal neurons, had acquired toleran ce in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distrib ution and the Ca2+ adenosine triphosphatase (Ca2+-ATPase) activity usi ng electron microscopic cytochemistry. In comparison with nonischemia- tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons se questered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapi dly decreased. Plasma membrane Ca2+-ATPase activities were already sig nificantly elevated before the 5 min of ischemia, and remained at a hi gher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca2+-ATPase activit ies in ischemia-tolerant CA1 neurons after the 5-min period of ischemi a showed a strong resemblance to those in CA3 neurons, which originall y possess resistance to such periods of ischemia. These findings sugge st that enhanced or maintained activities of mitochondrial Ca2+ seques tration and plasma membrane Ca2+-ATPase reduced Ca2+ toxicity followin g 5-min ischemia in terms of time, resulting in escape from delayed ne uronal death.