ArticleCNS neuroscience & therapeutics2026
Inhibition of Cerebellar Dentate Nucleus-Zona Incerta Glutamatergic Circuit Improves Sleep Disturbances in Chronic Temporal Lobe Epilepsy Model.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundPatients 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.
methodsThis 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.
resultsOur 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.
conclusionsTargeting the CDN-ZI glutamatergic circuit represents a promising therapeutic strategy for addressing sleep disorders resulting from chronic TLE.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.