Abstract

Epilepsy is a recurrent neurological disease caused by hypersynchronous firing of neurons in the brain. Neuronal apoptosis, microgliosis, or astrogliosis in hippocampus are considered to be important features of temporal lobe epilepsy. As an important part of the ventral striatum, the nucleus accumbens is closely connected to the hippocampus. As the findings of the reviewed articles indicated, the nuleus accumbens is divided into the shell and the core. The nucleus accumbens shell is a relevant brain region to process reward-related and motivated behaviours, emotional process and social information. Nucleus accumbens shell has a good application effect in the field of drug addiction and mania. Our previous studies have shown that the nucleus accumbens shows abnormal excitation after seizures. In our previous experiments, the number of seizures decreased when this excitation was disrupted. However, the mechanisms of action of Nucleus accumbens shell lesions remain unclear. In this paper, we explored the hippocampal changes inhibited by nucleus accumbens lesions on the basis of the kainic acid animal model of epilepsy. We explored the anti-epileptic effect and mechanism of action of electrical lesions in nucleus accumbens, and found that the mechanism may be to reduce the toxic effects caused by the proliferation of astrocytes and microglia in the hippocampus. It can also inhibit the reduction of neurons and thus play a role in controlling seizures. These results suggest that the nucleus accumbens plays an important role in inhibiting seizures.