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N-methyl-D-aspartate receptor functions altered by neuronal PTP1B activation in Alzheimer’s disease and schizophrenia models

N-methyl-D-aspartate receptor functions altered by neuronal PTP1B activation in Alzheimer’s disease and schizophrenia models

作     者:Alexandre F.R.Stewart Hsiao-Huei Chen Alexandre F.R.Stewart;Hsiao-Huei Chen

作者机构:Department of BiochemistryMicrobiology and ImmunologyUniversity of Ottawaand University of Ottawa Heart InstituteOttawaONCanada Centre for InfectionImmunity and InflammationOttawaONCanada MedicineCellular and Molecular MedicineUniversity of Ottawa Brain and Mind InstituteOttawa Hospital Research InstituteOttawaONCanada 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2022年第17卷第10期

页      面:2208-2210页

核心收录:

学科分类:0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100203[医学-老年医学] 100205[医学-精神病与精神卫生学] 10[医学] 

基  金:supported by grants from the Heart and Stroke Foundation of Canada(G-13-0002596&G-18-0022157,to HHC G-16-00014085,to AFRS) Ontario Mental Health Foundation(to HHC),the Canadian Institutes of Health Research(201610PJT#376403,to HHC 201610PJT#376503,to AFRS) the Natural Science and Engineering Research Council of Canada(RGPIN/06212-2014,to HHC RGPIN/2016-04985,to AFRS) supported by a Mid-Career Investigator Award(grant#7506)from the Heart and Stroke Foundation of Ontario. 

主  题:PTP1B aspartate NMDA 

摘      要:Glutamate is the main exc i tatory neurotransmitter in the brain and binds to two major classes of receptors,theα-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid(AMPA)and the N-methyl-D-aspartate(NMDA)receptors.Unlike AMPA receptors that are immediately activated by glutamate release,NMDA receptors are blocked by magnesium and can only be activated by glutamate after membrane depolarization.Thus,NMDA receptors are only activated after repeated AMPA receptor activation by glutamate.NMDA receptors are,for the most part,calcium-permeable channels.Calcium influx through NMDA receptors modulates synaptic transmission in neurons based on prior history of excitation,and provides a means of scaling the strength of synapses required for Hebbian plasticity.

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