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The Journal of Neurophysiology Vol. 82 No. 1 July 1999, pp. 382-397
Copyright ©1999 by the American Physiological Society
1Cellular and Systems Neurobiology Section,
Butera Jr., Robert J.,
John Rinzel, and
Jeffrey C. Smith.
Models of Respiratory Rhythm Generation in the
Pre-Bötzinger Complex. I. Bursting Pacemaker Neurons. J. Neurophysiol. 82: 382-397, 1999.
A network of
oscillatory bursting neurons with excitatory coupling is hypothesized
to define the primary kernel for respiratory rhythm generation in the
pre-Bötzinger complex (pre-BötC) in mammals. Two minimal
models of these neurons are proposed. In model 1, bursting
arises via fast activation and slow inactivation of a persistent
Na+ current INaP-h. In model
2, bursting arises via a fast-activating persistent
Na+ current INaP and slow activation of a
K+ current IKS. In both models, action
potentials are generated via fast Na+ and K+
currents. The two models have few differences in parameters to facilitate a rigorous comparison of the two different burst-generating mechanisms. Both models are consistent with many of the dynamic features of electrophysiological recordings from pre-BötC
oscillatory bursting neurons in vitro, including voltage-dependent
activity modes (silence, bursting, and beating), a voltage-dependent
burst frequency that can vary from 0.05 to >1 Hz, and a decaying spike frequency during bursting. These results are robust and persist across
a wide range of parameter values for both models. However, the dynamics
of model 1 are more consistent with experimental data in
that the burst duration decreases as the baseline membrane potential is
depolarized and the model has a relatively flat membrane potential
trajectory during the interburst interval. We propose several
experimental tests to demonstrate the validity of either model and to
differentiate between the two mechanisms.
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