Presented at the 20th International Epilepsy Congress, Oslo, July 3–8, 1993, and published in abstract form in Epilepsia 1993; 34(suppl 2):75.
Differential Impairments of Spatial Memory and Social Behavior in Two Models of Limbic Epilepsy
Article first published online: 3 AUG 2005
Volume 36, Issue 10, pages 973–982, October 1995
How to Cite
Letty, S., Lerner-Natoli, M. and Rondouin, G. (1995), Differential Impairments of Spatial Memory and Social Behavior in Two Models of Limbic Epilepsy. Epilepsia, 36: 973–982. doi: 10.1111/j.1528-1157.1995.tb00955.x
- Issue published online: 3 AUG 2005
- Article first published online: 3 AUG 2005
- Received October 1993; revision accepted March 8, 1995.
- Status epilepticus;
- Social interaction;
- Radial maze
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.