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The Journal of Neurophysiology Vol. 87 No. 5 May 2002, pp. 2307-2323
Copyright ©2002 by the American Physiological Society
1Faculty of Life Sciences, Gonda
(Goldschmied) Medical Diagnostic Research Center and
2Interdisciplinary Program in the Brain
Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel; and
3Department of Neurobiology and Anatomy, The
University of Texas
Houston Medical School, Houston, Texas 77030
Susswein, Abraham J.,
Itay Hurwitz,
Richard Thorne,
John H. Byrne, and
Douglas A. Baxter.
Mechanisms Underlying Fictive Feeding in Aplysia:
Coupling Between a Large Neuron With Plateau Potentials Activity and a
Spiking Neuron. J. Neurophysiol. 87: 2307-2323, 2002. The buccal ganglia of Aplysia contain a
central pattern generator (CPG) that organizes the rhythmic movements
of the radula and buccal mass during feeding. Many of the cellular and
synaptic elements of this CPG have been identified and characterized.
However, the roles that specific cellular and synaptic properties play in generating patterns of activity are not well understood. To examine
these issues, the present study developed computational models of a
portion of this CPG and used simulations to investigate processes
underlying the initiation of patterned activity. Simulations were done
with the SNNAP software package. The simulated network contained two
neurons, B31/B32 and B63. The development of the model was guided and
constrained by the available current-clamp data that describe the
properties of these two protraction-phase interneurons B31/B32 and B63,
which are coupled via electrical and chemical synapses. Several
configurations of the model were examined. In one configuration, a fast
excitatory postsynaptic potential (EPSP) from B63 to B31/B32 was
implemented in combination with an endogenous plateau-like potential in
B31/B32. In a second configuration, the excitatory synaptic connection
from B63 to B31/B32 produced both fast and slow EPSPs in B31/B32 and
the plateau-like potential was removed from B31/B32. Simulations
indicated that the former configuration (i.e., electrical and fast
chemical coupling in combination with a plateau-like potential) gave
rise to a circuit that was robust to changes in parameter values and
stochastic fluctuations, that closely mimicked empirical observations,
and that was extremely sensitive to inputs controlling the onset of a
burst. The coupling between the two simulated neurons served to amplify
exogenous depolarizations via a positive feedback loop and the
subthreshold activation of the plateau-like potential. Once a burst was
initiated, the circuit produced the program in an all-or-none fashion.
The slow kinetics of the simulated plateau-like potential played
important roles in both initiating and maintaining the burst activity.
Thus the present study identified cellular and network properties that
contribute to the ability of the simulated network to integrate
information over an extended period before a decision is made to
initiate a burst of activity and suggests that similar mechanisms may
operate in the buccal ganglia in initiating feeding movements.
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