We have constructed a detailed model of a hippocampal dentate granule (DG) cell that includes nine different channel types.
Channel densities and distributions were chosen to reproduce reported physiological responses observed in normal solution and when blockers were applied.
The model was used to explore the contribution of each channel type to spiking behavior with particular emphasis on the mechanisms underlying postspike events.
The model was used to predict changes in channel densities that could lead to epileptogenic burst discharges and to predict the effect of altered buffering capacity on firing behavior.
We conclude that the clustered spatial distributions of calcium related channels, the presence of slow delayed rectifier potassium currents in dendrites, and calcium buffering properties, together, might explain the resistance of DG cells to the development of epileptogenic burst discharges.
Aradi I, Holmes WR (1999) Role of multiple calcium and calcium-dependent conductances in regulation of hippocampal dentate granule cell excitability. J Comput Neurosci 6:215-35 [PubMed]