CNS neuroscience & therapeutics · 2026
Inhibition of Cerebellar Dentate Nucleus-Zona Incerta Glutamatergic Circuit Improves Sleep Disturbances in Chronic Temporal Lobe Epilepsy Model.
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Xia Liang, Wang Xuan, Zhang Yingchi, Hao Jianmin, Mi Dan, Song Changgeng, Jiang Wen
Аннотация
BACKGROUND: Patients with chronic temporal lobe epilepsy (TLE) frequently experience various sleep disorders, characterized by reduced sleep duration, diminished sleep stages, and disrupted sleep patterns. Recent research has identified a population of GABAergic neurons in the ventral zona incerta (ZI) that is instrumental in promoting sleep, along with a neural pathway that connects the cerebellar dentate nucleus (CDN) to the ZI. However, the precise role of this circuit in regulating sleep patterns remains inadequately understood.
METHODS: This study employed anatomical, chemogenetic, optogenetic, and immunofluorescence staining techniques to investigate the potential of the CDN-ZI circuit in ameliorating sleep disturbances associated with TLE.
RESULTS: Our findings indicate that pilocarpine-treated mice exhibit significant sleep fragmentation and reduced sleep duration, particularly during non-rapid eye movement sleep. By employing optogenetic and chemogenetic methods to target CDN glutamatergic neurons, we observed a decrease in sleep fragmentation, an increase in overall sleep duration, and an enhancement in sleep quality in pilocarpine-treated mice. The inhibition of the CDN-ZI glutamatergic circuit through optogenetic and chemogenetic methods resulted in substantial improvements in sleep disturbances following TLE.
CONCLUSIONS: Targeting the CDN-ZI glutamatergic circuit represents a promising therapeutic strategy for addressing sleep disorders resulting from chronic TLE.
METHODS: This study employed anatomical, chemogenetic, optogenetic, and immunofluorescence staining techniques to investigate the potential of the CDN-ZI circuit in ameliorating sleep disturbances associated with TLE.
RESULTS: Our findings indicate that pilocarpine-treated mice exhibit significant sleep fragmentation and reduced sleep duration, particularly during non-rapid eye movement sleep. By employing optogenetic and chemogenetic methods to target CDN glutamatergic neurons, we observed a decrease in sleep fragmentation, an increase in overall sleep duration, and an enhancement in sleep quality in pilocarpine-treated mice. The inhibition of the CDN-ZI glutamatergic circuit through optogenetic and chemogenetic methods resulted in substantial improvements in sleep disturbances following TLE.
CONCLUSIONS: Targeting the CDN-ZI glutamatergic circuit represents a promising therapeutic strategy for addressing sleep disorders resulting from chronic TLE.