Memory deficits after recovery of transient forebrain ischemia in rats: a preliminary report

RESUMO

Transient forebrain ischemia causes delayed cell death of vulnerable neuronal populations, in rodents, primates and man, mainly in the pyramidal CA1 sector of the hippocampus. Lesions involving hippocampal formation are of great interest due to its recognized importance in information processing. In a series of experiments, we investigated the performance of rats after recovery of an ischemic episode, in two avoidance tasks and in one appetitive task with a spatial component. Wistar rats were subjected to transient forebrain ischemia (ISC) through electrocauterization of vertebral arteries and 20 min occlusion of common carotids. One group was tested 21 to 28 days after ISC, and another 7 months after the episode, along with agematched controls. Ischemic animals tested in the early phase of recovery showed impairment of both inhibitory and active avoidance tasks, as well as the water-finding task. However, ischemic rats tested after long-term recovery exhibited avoidance deficits in the active, but not in the inhibitory task, and presented higher latencies of water-finding. Considering that the pattern of cognitive impairment after short and long recovery periods is different, we suggest that neuronal circuitry involved in the tasks studied may be influenced by the probable reorganization of hippocampal synapses after recovery from an ischemic episode.