ArticleEpileptic disorders : international epilepsy journal with videotape2025
Nucleus accumbens shell electrical lesion attenuates seizures and gliosis in chronic temporal lobe epilepsy rats.
Article in Epileptic disorders : international epilepsy journal with videotape, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Resting-State fMRI Functional Connectivity Alterations in Drug-Resistant Epilepsy Compared to Well-Controlled Epilepsy and Healthy Controls.Neurology international · 2026Article
- Nucleus accumbens shell electrical lesion attenuates seizures and gliosis in chronic temporal lobe epilepsy rats.Epileptic disorders : international epilepsy journal with videotape · 2025Article
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11 authors.
Funding
Abstract
objectiveTemporal lobe epilepsy (TLE) is the most prevalent form of epilepsy. Prior research has indicated the involvement of the nucleus accumbens shell (NAcSh) in the process of epileptogenesis, thereby implying its potential as a therapeutic target for TLE. In the present study, we investigated the antiepileptic effect of the NAcSh electrical lesion.
methodsChronic TLE was induced by stereotactic injection of kainic acid (KA) into the hippocampus 3 weeks after KA administration, and NAcSh electrical lesions were performed. Seizures in rats were monitored by video electroencephalogram (EEG) 1 week following the NAcSh electrical lesion. Besides, the spatial memory function assessment in rats was conducted using the Morris water maze (MWM) test in the final week of the experiment. Later, hippocampal glial cell activation and neuron loss in rats were evaluated through immunohistochemistry.
resultsTLE rats subjected to NAcSh electrical lesion exhibited a significant reduction in the frequency of seizures compared to untreated TLE rats. Furthermore, NAcSh electrical lesion led to less activation of hippocampal glial cells and fewer neuronal loss in TLE rats. It is worth noting that the NAcSh electrical lesion did not cause additional memory impairment. SIGNIFICANCE: In the present study, the NAcSh electrical lesion exhibited a definitive therapeutic effect on the chronic TLE rat model, potentially due to decreased hippocampal TLE-induced activation of glial cells and neuron loss. In conclusion, our results indicated that the NAcSh is a promising therapeutic target for TLE and possesses high potential for clinical application.
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