Differential Impairments of Spatial Memory and Social Behavior in Two Models of Limbic Epilepsy


  • Presented at the 20th International Epilepsy Congress, Oslo, July 3–8, 1993, and published in abstract form in Epilepsia 1993; 34(suppl 2):75.

Address correspondence and reprint requests to Dr. S. Letty at INSERM U249, CNRS UPR9008, Laboratoire de Médecine Expérimentale, Institut de Biologie, Bld. Henri IV, 34000 Montpellier, France.


Summary: To explore memory impairments in temporal lobe epilepsy, we used two experimental models in the rats: (a) kainate-induced status epilepticus (SE) resulting in excitotoxic damage and in later spontaneous seizures; and (b) amygdala kindling, known to induce no lesions (or only minor) and neuronal reorganization. Long-term effects of these models on memory were investigated with a spatial learning task in a radial-arm maze, and a social interaction test that implies degree of short-term memory. An histological analysis was made to determine neuronal damage or loss caused by epileptic activity in brain regions that could be related to memory functions. Kainate-induced epilepsy produced large memory deficits in animals tested 5 months after the injection. The rats showed severe lesions in amygdala and hippocampus and piriform and entorhinal cortex. Spatial memory was strongly diminished. The social memory test was severely impaired, probably due to the extent of amygdala injury, which is known to disturb social behavior. On the contrary, kindled rats showed no evident lesion in any brain region and displayed performances as good as those of controls in both tests. These experiments demonstrated that memory deficits appear to be related to the severity of neuronal damage in limbic areas, and the ability to develop seizures (permanence) is not solely responsible for these memory disturbances.