View in EDS PDF Full Text

Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders.

Saved in:
Bibliographic Details
Title: Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders.
Authors: Hardingham, Giles E., Bading, Hilmar
Source: Nature Reviews Neuroscience. Oct2010, Vol. 11 Issue 10, p682-696. 15p. 1 Black and White Photograph, 6 Diagrams.
Subjects: Methyl aspartate, Neurodegeneration, Neural receptors, Neural stimulation, Cell death, Etiology of diseases, Animal experimentation, Cell receptors, Cellular signal transduction, Comparative studies, Gene expression, Research methodology, Medical cooperation, Nervous system, Research, Oxidative stress, Evaluation research, Neuroprotective agents
Abstract: There is a long-standing paradox that NMDA (N-methyl-D-aspartate) receptors (NMDARs) can both promote neuronal health and kill neurons. Recent studies show that NMDAR-induced responses depend on the receptor location: stimulation of synaptic NMDARs, acting primarily through nuclear Ca(2+) signalling, leads to the build-up of a neuroprotective 'shield', whereas stimulation of extrasynaptic NMDARs promotes cell death. These differences result from the activation of distinct genomic programmes and from opposing actions on intracellular signalling pathways. Perturbations in the balance between synaptic and extrasynaptic NMDAR activity contribute to neuronal dysfunction in acute ischaemia and Huntington's disease, and could be a common theme in the aetiology of neurodegenerative diseases. Neuroprotective therapies should aim to both enhance the effect of synaptic activity and disrupt extrasynaptic NMDAR-dependent death signalling. [ABSTRACT FROM AUTHOR]
Copyright of Nature Reviews Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
FullText Links:
  – Type: pdflink
Text:
  Availability: 0
Header DbId: pbh
DbLabel: Psychology and Behavioral Sciences Collection
An: 53842616
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Hardingham%2C+Giles+E%2E%22">Hardingham, Giles E.</searchLink><br /><searchLink fieldCode="AR" term="%22Bading%2C+Hilmar%22">Bading, Hilmar</searchLink>
– Name: TitleSource
  Label: Source
  Group: Src
  Data: <searchLink fieldCode="JN" term="%22Nature+Reviews+Neuroscience%22">Nature Reviews Neuroscience</searchLink>. Oct2010, Vol. 11 Issue 10, p682-696. 15p. 1 Black and White Photograph, 6 Diagrams.
– Name: Subject
  Label: Subjects
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Methyl+aspartate%22">Methyl aspartate</searchLink><br /><searchLink fieldCode="DE" term="%22Neurodegeneration%22">Neurodegeneration</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+receptors%22">Neural receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+stimulation%22">Neural stimulation</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+death%22">Cell death</searchLink><br /><searchLink fieldCode="DE" term="%22Etiology+of+diseases%22">Etiology of diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Animal+experimentation%22">Animal experimentation</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+receptors%22">Cell receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Cellular+signal+transduction%22">Cellular signal transduction</searchLink><br /><searchLink fieldCode="DE" term="%22Comparative+studies%22">Comparative studies</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Research+methodology%22">Research methodology</searchLink><br /><searchLink fieldCode="DE" term="%22Medical+cooperation%22">Medical cooperation</searchLink><br /><searchLink fieldCode="DE" term="%22Nervous+system%22">Nervous system</searchLink><br /><searchLink fieldCode="DE" term="%22Research%22">Research</searchLink><br /><searchLink fieldCode="DE" term="%22Oxidative+stress%22">Oxidative stress</searchLink><br /><searchLink fieldCode="DE" term="%22Evaluation+research%22">Evaluation research</searchLink><br /><searchLink fieldCode="DE" term="%22Neuroprotective+agents%22">Neuroprotective agents</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: There is a long-standing paradox that NMDA (N-methyl-D-aspartate) receptors (NMDARs) can both promote neuronal health and kill neurons. Recent studies show that NMDAR-induced responses depend on the receptor location: stimulation of synaptic NMDARs, acting primarily through nuclear Ca(2+) signalling, leads to the build-up of a neuroprotective 'shield', whereas stimulation of extrasynaptic NMDARs promotes cell death. These differences result from the activation of distinct genomic programmes and from opposing actions on intracellular signalling pathways. Perturbations in the balance between synaptic and extrasynaptic NMDAR activity contribute to neuronal dysfunction in acute ischaemia and Huntington's disease, and could be a common theme in the aetiology of neurodegenerative diseases. Neuroprotective therapies should aim to both enhance the effect of synaptic activity and disrupt extrasynaptic NMDAR-dependent death signalling. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Nature Reviews Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=pbh&AN=53842616
RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1038/nrn2911
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 15
        StartPage: 682
    Subjects:
      – SubjectFull: Methyl aspartate
        Type: general
      – SubjectFull: Neurodegeneration
        Type: general
      – SubjectFull: Neural receptors
        Type: general
      – SubjectFull: Neural stimulation
        Type: general
      – SubjectFull: Cell death
        Type: general
      – SubjectFull: Etiology of diseases
        Type: general
      – SubjectFull: Animal experimentation
        Type: general
      – SubjectFull: Cell receptors
        Type: general
      – SubjectFull: Cellular signal transduction
        Type: general
      – SubjectFull: Comparative studies
        Type: general
      – SubjectFull: Gene expression
        Type: general
      – SubjectFull: Research methodology
        Type: general
      – SubjectFull: Medical cooperation
        Type: general
      – SubjectFull: Nervous system
        Type: general
      – SubjectFull: Research
        Type: general
      – SubjectFull: Oxidative stress
        Type: general
      – SubjectFull: Evaluation research
        Type: general
      – SubjectFull: Neuroprotective agents
        Type: general
    Titles:
      – TitleFull: Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders.
        Type: main
  BibRelationships:
    HasContributorRelationships:
      – PersonEntity:
          Name:
            NameFull: Hardingham, Giles E.
      – PersonEntity:
          Name:
            NameFull: Bading, Hilmar
    IsPartOfRelationships:
      – BibEntity:
          Dates:
            – D: 01
              M: 10
              Text: Oct2010
              Type: published
              Y: 2010
          Identifiers:
            – Type: issn-print
              Value: 1471003X
          Numbering:
            – Type: volume
              Value: 11
            – Type: issue
              Value: 10
          Titles:
            – TitleFull: Nature Reviews Neuroscience
              Type: main
ResultId 1