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CA1 pyramidal cell: I_NaP and I_M contributions to somatic bursting (Golomb et al 2006)
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To study the mechanisms of bursting, we have constructed a conductance-based, one-compartment model of CA1 pyramidal neurons. In this neuron model, reduced [Ca2+]o is simulated by negatively shifting the activation curve of the persistent Na+ current (INaP), as indicated by recent experimental results. The neuron model accounts, with different parameter sets, for the diversity of firing patterns observed experimentally in both zero and normal [Ca2+]o. Increasing INaP in the neuron model induces bursting and increases the number of spikes within a burst, but is neither necessary nor sufficient for bursting. We show, using fast-slow analysis and bifurcation theory, that the M-type K+ current (IM) allows bursting by shifting neuronal behavior between a silent and a tonically-active state, provided the kinetics of the spike generating currents are sufficiently, though not extremely, fast. We suggest that bursting in CA1 pyramidal cells can be explained by a single compartment *square bursting* mechanism with one slow variable, the activation of IM. See paper for more and details.
Golomb D, Yue C, Yaari Y (2006) Contribution of persistent Na+ current and M-type K+ current to somatic bursting in CA1 pyramidal cells: combined experimental and modeling study.
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Neuron or other electrically excitable cell;
Hippocampus CA1 pyramidal GLU cell;
Golomb, David [golomb at bgu.ac.il];
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Hippocampus CA1 pyramidal GLU cell
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