Ischemia-induced irreversible deficit of memory function in gerbils.

Ischemia for 5 min temporarily increased locomotor activity in gerbils after 1 and 3 days. Temporary increases were also noted within 7 and 5 days after 20-min ischemia and repeated ischemia (three 2-min ischemia at 1-h intervals), respectively. In a passive avoidance task, gerbils were trained 2 or 14 days before the occlusion and then tested 1 day after it. Shortened step-through latency was observed in the retention test 3 days after 5-min ischemia, but not after 15 days (reversible deficit). In contrast, following 20-min ischemia, the step-through latency was significantly lower after 3 days and also after 15 days (irreversible deficit). Working memory was also tested with gerbils trained for an 8-arm radial maze task. A significantly higher working error was observed 1 day after 5-min ischemia but not after 5 days (reversible deficit). However, ischemia for 20-min and repeated ischemia led to markedly increase working error 1 day after the occlusion, with significant increases even after 14 and 28 days (irreversible deficit). In addition, while 5-min ischemia occurred the neuronal death in the hippocampal CA1 subfield, 20-min ischemia produced it not only in the CA1 subfield but also in the CA2-4 subfield and dorsal striatum. These results indicated that 5-min ischemia led to a reversible memory deficit, while 20-min and repeated ischemia produced an irreversible deficit.