Regulation of NMDA receptor Ca2+ signalling and synaptic plasticity

C. Geoffrey Lau, Koichi Takeuchi, Alma Rodenas-Ruano, Yukihiro Takayasu, Jessica Murphy, Michael V.I. Bennett, R. Suzanne Zukin

Research output: Contribution to journalArticle

50 Scopus citations

Abstract

NMDARs (N-methyl-D-aspartate receptors) are critical for synaptic function throughout the CNS (central nervous system). NMDAR-mediated Ca2+ in.ux 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.

Original languageEnglish (US)
Pages (from-to)1369-1374
Number of pages6
JournalBiochemical Society transactions
Volume37
Issue number6
DOIs
StatePublished - Nov 27 2009

Keywords

  • Calcium
  • N-methyl-d-aspartate receptor (NMDAR)
  • Protein kinase
  • Signalling
  • Synaptic plasticity

ASJC Scopus subject areas

  • Biochemistry

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