NMDA receptors (NMDA-R) typically contribute to excitatory synaptic transmission in the central nervous system. While calcium influx through NMDA-R plays a critical role in synaptic plasticity, indirect experimental evidence also exists demonstrating actions of NMDAR-mediated calcium influx on neuronal excitability through the activation of calcium-activated potassium channels. But, so far, this mechanism has not  been studied theoretically. Our theoretical model provide a simple description of neuronal electrical activity including the tonic activity of  NMDA receptors and a cytosolic calcium compartment. We show that calcium influx through NMDA-R can directly be coupled to activation of calcium-activated potassium channels providing an overall inhibitory effect on neuronal excitability. Furthermore, the presence of tonic NMDA-R activity promotes bistability in electrical activity by dramatically increasing the stimulus interval where both a stable steady state and repetitive firing can exist. This results could provide an intrinsic mechanism for the constitution of memory traces in neuronal circuits. They also shed light on the way by which beta-amyloids can decrease neuronal activity when interfering with NMDA-R in Alzheimer's disease  .
NMDA receptors (NMDA-R) typically contribute to excitatory synaptic transmission in the central nervous system. While calcium influx through NMDA-R plays a critical role in synaptic plasticity, experimental evidence indicates that NMDAR-mediated calcium influx also modifies neuronal excitability through the activation of calcium-activated potassium channels. This mechanism has not yet been studied theoretically. Our theoretical model provides a simple description of neuronal electrical activity that takes into account the tonic activity of extrasynaptic NMDA receptors and a cytosolic calcium compartment. We show that calcium influx mediated by the tonic activity of NMDA-R can be coupled directly to the activation of calcium-activated potassium channels , resulting in an overall inhibitory effect on neuronal excitability. Furthermore, the presence of tonic NMDA-R activity promotes bistability in electrical activity by dramatically increasing the stimulus interval where both a stable steady state and repetitive firing can coexist. These results could provide an intrinsic mechanism for the constitution of memory traces in neuronal circuits. They also shed light on the way by which \beta-amyloids can alter neuronal activity when interfering with NMDA-R in Alzheimer's disease and cerebral ischemia .
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