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.
Reference:
1 .
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. J Neurophysiol 96:1912-26 [PubMed]
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