Journal
NATURE REVIEWS NEUROSCIENCE
Volume 11, Issue 10, Pages 682-696Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn2911
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Funding
- Wellcome Trust
- Medical Research Council (MRC)
- Biotechnology and Biological Sciences Research Council
- Royal Society
- Alexander von Humboldt Foundation
- European Research Council
- Deutsche Forschungsgemeinschaft
- EU
- MRC [G0902044] Funding Source: UKRI
- Medical Research Council [G0902044] Funding Source: researchfish
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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 Ca2+ 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.
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