A network of oscillatory bursting neurons with excitatory coupling is hypothesized to define the primary kernel for respiratory rhythm
generation in the pre-Botzinger complex (pre-BotC) 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 K1 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-BotC 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.
Reference:
1 .
Butera RJ, Rinzel J, Smith JC (1999) Models of respiratory rhythm generation in the pre-Bötzinger complex. I. Bursting pacemaker neurons. J Neurophysiol 82:382-97 [PubMed]
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