The model is based on that of Aradi & Holmes (1999; Journal of Computational Neuroscience 6, 215-235). It was used to help understand the contribution of M and SK channels to the medium afterhyperpolarization (mAHP) following one or seven spikes, as well as the contribution of M channels to the slow afterhyperpolarization (sAHP). We found that SK channels are the main determinants of the mAHP, in contrast to CA1 pyramidal cells where the mAHP is primarily caused by the opening of M channels. The model reproduced these experimental results, but we were unable to reproduce the effects of the M-channel blocker XE991 on the sAHP. It is suggested that either the XE991-sensitive component of the sAHP is not due to M channels, or that when contributing to the sAHP, these channels operate in a mode different from that associated with the mAHP.
Model Type: Neuron or other electrically excitable cell; Axon; Channel/Receptor; Dendrite
Cell Type(s): Dentate gyrus granule GLU cell
Currents: I Na,t; I L high threshold; I N; I T low threshold; I A; I K; I M; I K,Ca; I Sodium; I Calcium; I Potassium
Model Concept(s): Ion Channel Kinetics; Detailed Neuronal Models; Action Potentials; Calcium dynamics; Spike Frequency Adaptation; Conductance distributions
Simulation Environment: NEURON
Implementer(s): Murphy, Ricardo [ricardo.murphy at medisin.uio.no]
References:
Mateos-Aparicio P, Murphy R, Storm JF. (2014). Complementary functions of SK and Kv7/M potassium channels in excitability control and synaptic integration in rat hippocampal dentate granule cells. The Journal of physiology. 592 [PubMed]