Effect of accumbens nucleus shell lesioning on bitemporal lobe epilepsy in rat model.

Abstract

INTRODUCTION: To explore the effect of accumbens nucleus shell (ACbSh) lesioning on bitemporal lobe epilepsy. MATERIAL AND METHODS: Adult Wistar rats (male) were enrolled and randomly assigned into the control group and epilepsy groups with multiple time-points. Lithium-pilocarpine was used to establish the rat epilepsy model, while the control group received an equal amount of saline. Ibotenic acid stereotaxic injection was performed to cause accumbens nucleus shell lesioning for specific groups. Cascade software was used for electroencephalogram (EEG) examination. Fluoro-Jade C staining was performed to examine neuronal degeneration. RESULTS: Latency period of the epilepsy in epilepsy groups was 15.3 &#xb1; 1.1 min, and epilepsy intensity was 4.8 &#xb1; 0.5 events/ 12 h. ACbSh lesioning significantly reduced aggressive behavior. Compared with epilepsy groups without ACbSh lesioning, ACbSh lesioning significantly decreased epileptic seizures and reduced epileptic duration (p < 0.05). EEG showed that there were still sharp waves in the hippocampus and amygdala region after ACbSh lesioning, but epileptic discharge in prefrontal cortex was significantly decreased (p < 0.05), while epilepsy groups without ACbSh lesioning had more sharp waves in the prefrontal cortex, hippocampus and amygdala region. Fluoro-Jade C staining showed that ACbSh lesioning significantly decreased grades of neuronal degeneration (p < 0.05). CONCLUSIONS: Recurrent epilepsy caused neuronal degeneration via ACbSh region-related pathways, and ACbSh lesioning could mitigate epilepsy-caused neuronal degeneration by reducing epileptic discharge.