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

被引：29
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
来源：
CNS NEUROSCIENCE & THERAPEUTICS | 2022年 / 28卷 / 09期
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 [J].
Albrecht, Jan ;
Zielinska, Magdalena .
NEUROCHEMICAL RESEARCH, 2017, 42 (06) :1724-1734
[2]   NA,K-ATPASE IS DECREASED IN HIPPOCAMPUS OF KAINATE-LESIONED RATS [J].
ANDERSON, WR ;
FRANCK, JE ;
STAHL, WL ;
MAKI, AA .
EPILEPSY RESEARCH, 1994, 17 (03) :221-231
[3]   Diseases caused by mutations in the Na+/K+ pump α1 gene ATP1A1 [J].
Biondo, Elisa D. ;
Spontarelli, Kerri ;
Ababioh, Giovanna ;
Mendez, Lois ;
Artigas, Pablo .
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 [J].
Blanco, G .
SEMINARS IN NEPHROLOGY, 2005, 25 (05) :292-303
[5]   In and out of the cation pumps: P-Type ATPase structure revisited [J].
Bublitz, Maike ;
Poulsen, Hanne ;
Morth, J. Preben ;
Nissen, Poul .
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 [J].
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 .
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 [J].
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. .
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 [J].
Condon, Kendall J. ;
Sabatini, David M. .
JOURNAL OF CELL SCIENCE, 2019, 132 (21)
[10]   Alternating Hemiplegia of Childhood: Genotype-Phenotype Correlations in a Cohort of 39 Italian Patients [J].
Cordani, Ramona ;
Stagnaro, Michela ;
Pisciotta, Livia ;
Tiziano, Francesco Danilo ;
Calevo, Maria Grazia ;
Nobili, Lino ;
De Grandis, Elisa .
FRONTIERS IN NEUROLOGY, 2021, 12
123456789