The paper argues for competing roles of NR2A- and NR2B-containing NMDARs in spike-timing-dependent plasticity. This simple dynamical model recapitulates the results of STDP experiments involving selective blockers of NR2A- and NR2B-containing NMDARs, for which the stimuli are pre- and postsynaptic spikes in varying combinations. Experiments were done using paired recordings from glutamatergic neurons in rat hippocampal cultures. This model focuses on the dynamics of the putative potentiation and depression modules themselves, and their interaction For detailed dynamics involving NMDARs and Ca2+ transients, see Rubin et al., J. Neurophys., 2005.
Model Type: Synapse
Cell Type(s): Hippocampus CA1 pyramidal GLU cell; Hippocampus CA3 pyramidal GLU cell
Receptors: NMDA
Genes: NR2A GRIN2A; NR2B GRIN2B
Model Concept(s): Activity Patterns; Synaptic Plasticity; Long-term Synaptic Plasticity; Signaling pathways; Synaptic Integration; Winner-take-all; STDP
Simulation Environment: IGOR Pro
References:
Gerkin RC, Lau PM, Nauen DW, Wang YT, Bi GQ. (2007). Modular competition driven by NMDA receptor subtypes in spike-timing-dependent plasticity. Journal of neurophysiology. 97 [PubMed]