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- W2022873534 endingPage "1374" @default.
- W2022873534 startingPage "1369" @default.
- W2022873534 abstract "NMDARs (N-methyl-D-aspartate receptors) are critical for synaptic function throughout the CNS (central nervous system). NMDAR-mediated Ca2+ influx is implicated in neuronal differentiation, neuronal migration, synaptogenesis, structural remodelling, long-lasting forms of synaptic plasticity and higher cognitive functions. NMDAR-mediated Ca2+ signalling in dendritic spines is not static, but can be remodelled in a cell- and synapse-specific manner by NMDAR subunit composition, protein kinases and neuronal activity during development and in response to sensory experience. Recent evidence indicates that Ca2+ permeability of neuronal NMDARs, NMDAR-mediated Ca2+ signalling in spines and induction of NMDAR-dependent LTP (long-term potentiation) at hippocampal Schaffer collateral–CA1 synapses are under control of the cAMP/PKA (protein kinase A) signalling cascade. Thus, by enhancing Ca2+ influx through NMDARs in spines, PKA can regulate the induction of LTP. An emerging concept is that activity-dependent regulation of NMDAR-mediated Ca2+ signalling by PKA and by extracellular signals that modulate cAMP or protein phosphatases at synaptic sites provides a dynamic and potentially powerful mechanism for bi-directional regulation of synaptic efficacy and remodelling." @default.
- W2022873534 created "2016-06-24" @default.
- W2022873534 creator A5014646633 @default.
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- W2022873534 date "2009-11-19" @default.
- W2022873534 modified "2023-09-30" @default.
- W2022873534 title "Regulation of NMDA receptor Ca2+ signalling and synaptic plasticity" @default.
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- W2022873534 doi "https://doi.org/10.1042/bst0371369" @default.
- W2022873534 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3501105" @default.