The Yin and Yang of NMDA receptor signalling.
By G. Hardingham, Hilmar Bading. Trends in Neurosciences, 2003
667 citations recorded by the source corpus.
Subfields: Cell Biology, Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/ec6fc9e4445aadca81660400c173c07abb20d366
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In Cell Biology
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In Cognitive Neuroscience
Citations in the corpus
- A peptide inhibitor of c-Jun N-terminal kinase protects against excitotoxicity and cerebral ischemia (2003, background): “Alternatively, the lesser protection by glutamate antagonists might be a result of their inhibition of survival pathways not affected by the peptide”
- Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients (2006, background): “It is possible that this microglial response is initially neuroprotective as reducing inhibitory innervation of motor neurons increases firing of synaptic NMDA (N-methyl-D-aspartate) receptors and inhibits cell death pathways by triggering cAMP-response element binding protein (CREB) activity and br”
- Synaptic and extrasynaptic NMDA receptors are gated by different endogenous coagonists. (2012, result): “They are, however, in strong disagreement with those obtained in cultured neurons (Hardingham et al., 2002; Hardingham and Bading, 2003; Léveillé et al., 2008) reporting a preferential role for extrasynaptic NMDARs in excitotoxicity.”
- Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders (2010, neutral): “According to this model, neuronal responses to NMDAR activity follow a bell-shaped curve, in which both too much and too little response is potentially harmfu”
- Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms (2008, background): “It has been proposed that robust activation of extrasynaptic NMDA receptors may be an important contributor to excitotoxic cell death (Hardingham and Bading, 2003).”