Potentiation of Ca2+ influx through NMDA channels by action potentials: a computer model.
In pyramidal cells, somatic action potentials can propagate actively back into the apical dendrites and potentiate calcium influx at simultaneously activated glutamatergic synapses, presumably by relieving the voltage-dependent block of NMDA channels. We have used computer simulations to investigate the conditions under which this potentiation will be optimal. We find that a spike with a long duration and limited amplitude (peak of approximately -10 mV) will be most effective. A back-propagating action potential will achieve this form if the dendritic membrane has a low K+ channel density and a modest Na+ channel density (30-70 pS/microm2, similar to experimentally observed densities). The relative increase in calcium due to the backpropagating spike will be small, however, unless the accumulated calcium is rapidly removed.
Neville
K R
KR
Neuroscience Training Program, University of Wisconsin-Madison, 53706, USA.
Lytton
W W
WW
D000200:Action Potentials / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D003198:Computer Simulation; D003712:Dendrites / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D007700:Kinetics; D017774:Long-Term Potentiation / Q000502:physiology; D008959:Models, Neurological; D015221:Potassium Channels / Q000378:metabolism; D017966:Pyramidal Cells / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D015222:Sodium Channels / Q000378:metabolism; D012984:Software; D009435:Synaptic Transmission
D015221:Potassium Channels; D016194:Receptors, N-Methyl-D-Aspartate; D015222:Sodium Channels; D002118:Calcium