The role of Na+-K+-ATPase in the epileptic brain

被引:27
作者
Sun, Jinyi [1 ]
Zheng, Yang [2 ]
Chen, Zhong [1 ,2 ,3 ]
Wang, Yi [1 ,2 ,3 ]
机构
[1] Zhejiang Univ, Inst Pharmacol & Toxicol, Coll Pharmaceut Sci, Hangzhou 310058, Peoples R China
[2] Zhejiang Chinese Med Univ, Sch Pharmaceut Sci, Key Lab Neuropharmacol & Translat Med Zhejiang Pr, Hangzhou, Peoples R China
[3] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Epilepsy Ctr,Dept Neurol, Hangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
drug target; epilepsy; excitability; Na plus -K plus -ATPase; FAMILIAL HEMIPLEGIC MIGRAINE; DE-NOVO MUTATIONS; CRYSTAL-STRUCTURE; CEREBRAL-CORTEX; P2X7; RECEPTOR; ATP1A2; NA; K-ATPASE; NA+; K+-ATPASE; PILOCARPINE; SEIZURES;
D O I
10.1111/cns.13893
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Na+-K+-ATPase, a P-type ATP-powered ion transporter on cell membrane, plays a vital role in cellular excitability. Cellular hyperexcitability, accompanied by hypersynchronous firing, is an important basis for seizures/epilepsy. An increasing number of studies point to a significant contribution of Na+-K+-ATPase to epilepsy, although discordant results exist. In this review, we comprehensively summarize the structure and physiological function of Na+-K+-ATPase in the central nervous system and critically evaluate the role of Na+-K+-ATPase in the epileptic brain. Importantly, we further provide perspectives on some possible research directions and discuss its potential as a therapeutic target for the treatment of epilepsy.
引用
收藏
页码:1294 / 1302
页数:9
相关论文
共 90 条
  • [1] Mechanisms of Excessive Extracellular Glutamate Accumulation in Temporal Lobe Epilepsy
    Albrecht, Jan
    Zielinska, Magdalena
    [J]. NEUROCHEMICAL RESEARCH, 2017, 42 (06) : 1724 - 1734
  • [2] NA,K-ATPASE IS DECREASED IN HIPPOCAMPUS OF KAINATE-LESIONED RATS
    ANDERSON, WR
    FRANCK, JE
    STAHL, WL
    MAKI, AA
    [J]. EPILEPSY RESEARCH, 1994, 17 (03) : 221 - 231
  • [3] Diseases caused by mutations in the Na+/K+ pump α1 gene ATP1A1
    Biondo, Elisa D.
    Spontarelli, Kerri
    Ababioh, Giovanna
    Mendez, Lois
    Artigas, Pablo
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2021, 321 (02): : C394 - C408
  • [4] Na,K-ATPase subunit heterogeneity as a mechanism for tissue-specific ion regulation
    Blanco, G
    [J]. SEMINARS IN NEPHROLOGY, 2005, 25 (05) : 292 - 303
  • [5] In and out of the cation pumps: P-Type ATPase structure revisited
    Bublitz, Maike
    Poulsen, Hanne
    Morth, J. Preben
    Nissen, Poul
    [J]. CURRENT OPINION IN STRUCTURAL BIOLOGY, 2010, 20 (04) : 431 - 439
  • [6] BURNSTOCK G, 1972, PHARMACOL REV, V24, P509
  • [7] A novel lethal recognizable polymicrogyric syndrome caused by ATP1A2 homozygous truncating variants
    Chatron, Nicolas
    Cabet, Sara
    Alix, Eudeline
    Buenerd, Annie
    Cox, Phillip
    Guibaud, Laurent
    Labalme, Audrey
    Marks, Peter
    Osio, Deborah
    Putoux, Audrey
    Sanlaville, Damien
    Lesca, Gaetan
    Vasiljevic, Alexandre
    [J]. BRAIN, 2019, 142 : 3367 - 3374
  • [8] Mutation I810N in the α3 isoform of Na+,K+-ATPase causes impairments in the sodium pump and hyperexcitability in the CNS
    Clapcote, Steven J.
    Duffy, Steven
    Xie, Gang
    Kirshenbaum, Greer
    Bechard, Allison R.
    Schack, Vivien Rodacker
    Petersen, Janne
    Sinai, Laleh
    Saab, Bechara J.
    Lerch, Jason P.
    Minassian, Berge A.
    Ackerley, Cameron A.
    Sled, John G.
    Cortez, Miguel A.
    Henderson, Jeffrey T.
    Vilsen, Bente
    Roder, John C.
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (33) : 14085 - 14090
  • [9] Nutrient regulation of mTORC1 at a glance
    Condon, Kendall J.
    Sabatini, David M.
    [J]. JOURNAL OF CELL SCIENCE, 2019, 132 (21)
  • [10] Alternating Hemiplegia of Childhood: Genotype-Phenotype Correlations in a Cohort of 39 Italian Patients
    Cordani, Ramona
    Stagnaro, Michela
    Pisciotta, Livia
    Tiziano, Francesco Danilo
    Calevo, Maria Grazia
    Nobili, Lino
    De Grandis, Elisa
    [J]. FRONTIERS IN NEUROLOGY, 2021, 12