Evidence map›Paper›PMID 39042219›Full record

ArticleMolecular neurobiology2025

Deep Brain Stimulation Inhibits Epileptic Seizures via Increase of Adenosine Release and Inhibition of ENT1, CD39, and CD73 Expression.

Zhonghua Xiong, Jiahui Deng, Pandeng Xie, Chongyang Tang, Jing Wang, Qinqin Deng, Yujiao Yang, Jing Zhang, Mengyi Guo, Xiongfei Wang and 4 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Microglial Feimin Alleviates Cognitive Impairment in High-Fat Diet-Fed Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Zhonghua Xiong *Department of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jiahui Deng *Department of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Pandeng XieDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Chongyang TangDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jing WangDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Qinqin DengDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Yujiao YangDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jing ZhangDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Mengyi GuoDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Xiongfei WangDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Yuguang GuanDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Guoming LuanDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jian ZhouDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Tianfu LiDepartment of Brian Institute, Center of Epilepsy, Key Laboratory of Epilepsy Research, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China. tianfuli@ccmu.edu.cn.

Funding

National Key Research and Development Program of China No. 2021YFC2401203National Natural Science Foundation of China 81571275
6 · The paper itself

Abstract

Deep brain stimulation (DBS) of the anterior nucleus of the thalamus is an efficacious treatment option for patients with refractory epilepsy. Our previous study demonstrates that adenosine is a potential target of DBS for the treatment of epilepsy. Equilibrative nucleoside transporters-1 (ENT1) and ectonucleotidases (CD39, CD73) function as regulators of extracellular adenosine in the brain. It is unclear whether ENT1, CD39, and CD73 are involved in the mechanism of DBS for epilepsy. A total of 48 SD male rats were divided into four groups: control (naïve rats), Pilo (pilocarpine induced rats with epilepsy), DBS (rats with epilepsy treated with DBS for 8 weeks), and sham. In the present study, video electroencephalogram monitoring, Morris water maze assays, in vivo measurements of adenosine using fiber photometry, histochemistry, and western blot were performed on the hippocampus. DBS markedly attenuated spontaneous recurrent seizures (SRSs) and enhanced spatial learning in rats with epilepsy, assessed through video-EEG and water maze assays. Fibred photometry measurements of an adenosine sensor revealed dynamic increase in extracellular adenosine during DBS. The expressions of ENT1, CD39, and CD73 in Pilo group and sham group increased compared with the control group, while the expressions of ENT1, CD39, and CD73 in DBS group decreased compared to that of Pilo group and sham group. The findings indicate that DBS reduces the number of SRSs and improves spatial memory in rats with epilepsy with concomitant decrease of ENT1, CD39, and CD73 expressions. Adenosine-modulating enzymes might be the potential targets of DBS for the treatment of epilepsy.

Indexed as

5'-NucleotidaseAdenosineAntigens, CDApyraseDeep Brain StimulationEpilepsyEquilibrative Nucleoside Transporter 1SeizuresAnimalsHippocampusMaleRatsRats, Sprague-Dawley5'-NucleotidaseAdenosineAntigens, CDApyraseCD39 antigenEquilibrative Nucleoside Transporter 1Slc29a1 protein, ratAdenosineCD39CD73Deep brain stimulationENT1Epilepsy

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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.