Abstract
Large lesions (49.7–70.2%) of the hippocampus of rats reduced spontaneous alternation at minimal intertrial delay intervals to chance values, significantly less than the means of control groups, when animals were first tested postoperatively after 30 or 56 days of recovery. After 8 consecutive days of repeated testing, however, performance of the operated animals had improved and was not distinguishable from that of the controls. Upon introduction of a 10-s delay between trials, spontaneous alternation scores of operated rats returned to chance values, significantly less than the mean of the controls; the impairment was not ameliorated by repeated testing. These results contradict the internal inhibition hypothesis, which proposes that hippocampal damage affects the motivation to perform spontaneous alternation, and indicate that the spontaneous alternation deficit may be due to memory loss.
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