中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (7): 1417-1422.doi: 10.4103/1673-5374.360281

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

神经胶质细胞能拯救癫痫患者的神经元吗? 

  


  • 出版日期:2023-07-15 发布日期:2023-01-11

Can glial cells save neurons in epilepsy?

Weida Shen1, #, Jelena Bogdanović Pristov2, #, Paola Nobili3, *, Ljiljana Nikolić4, *   

  1. 1Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Zhejiang University City College, Hangzhou, Zhejiang Province, China; 2Department of Life Sciences, University of Belgrade, Institute for Multidisciplinary Research, Belgrade, Serbia; 3Institute of Functional Genomics (IGF), University of Montpellier, CNRS, INSERM, Montpellier, France; 4Department of Neurophysiology, Institute for Biological Research Siniša Stanković, National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia
  • Online:2023-07-15 Published:2023-01-11
  • Contact: Paola Nobili, PhD, paola.nobili@igf.cnrs.fr or pabela8207@gmail.com; Ljiljana Nikolić, PhD, nikolic13@gmail.com or ljnikolic@ibiss.bg.ac.rs.
  • Supported by:
    This work was supported by the Ministry of Education, Science and Technological Development of Republic of Serbia, Nos. 451-03-68/2022-14/200007 and 451-03-68/2022-14/200053 (to LN and JBP), Grants from European Commission (H2020 MSCA-ITN EU-GliaPhD No. 72205) (to PN), Agence Nationale de la Recherche, Nos. ANR-19-CE16-0018-03 and ANR-20CE16-0003-02 (to PN), Grants from Science and Technology Department of Zhejiang Province, China, No. 2021RC051 (to WS), and Scientific Research Foundation for Returned Scholars of Hangzhou City, China, No. 2019 (to WS).

摘要: http://orcid.org/0000-0003-2313-4223 (Paola Nobili); http://orcid.org/0000-0002-8575-7824 (Ljiljana Nikolić)

Abstract: Epilepsy is a neurological disorder caused by the pathological hyper-synchronization of neuronal discharges. The fundamental research of epilepsy mechanisms and the targets of drug design options for its treatment have focused on neurons. However, approximately 30% of patients suffering from epilepsy show resistance to standard anti-epileptic chemotherapeutic agents while the symptoms of the remaining 70% of patients can be alleviated but not completely removed by the current medications. Thus, new strategies for the treatment of epilepsy are in urgent demand. Over the past decades, with the increase in knowledge on the role of glia in the genesis and development of epilepsy, glial cells are receiving renewed attention. In a normal brain, glial cells maintain neuronal health and in partnership with neurons regulate virtually every aspect of brain function. In epilepsy, however, the supportive roles of glial cells are compromised, and their interaction with neurons is altered, which disrupts brain function. In this review, we will focus on the role of glia-related processes in epileptogenesis and their contribution to abnormal neuronal activity, with the major focus on the dysfunction of astroglial potassium channels, water channels, gap junctions, glutamate transporters, purinergic signaling, synaptogenesis, on the roles of microglial inflammatory cytokines, microglia-astrocyte interactions in epilepsy, and on the oligodendroglial potassium channels and myelin abnormalities in the epileptic brain. These recent findings suggest that glia should be considered as the promising next-generation targets for designing anti-epileptic drugs that may improve epilepsy and drug-resistant epilepsy.

Key words: astrocyte, cytokines, glutamate, ion channel, microglia, myelin, neuron, oligodendrocyte, purinergic signaling, seizures