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J Neurophysiol (January 1, 2003). 10.1152/jn.00729.2002
Submitted on Submitted 26 August 2002; accepted in final form 20 September 2002
1Department of Physics, University of Ottawa, Ottawa, Ontario K1N 6N5; 2Neuroscience Research Group, Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, T2N 4N1 Canada
Doiron, Brent,
Liza Noonan,
Neal Lemon, and
Ray W. Turner.
Persistent Na+ Current Modifies Burst Discharge By
Regulating Conditional Backpropagation of Dendritic Spikes. J. Neurophysiol. 89: 324-337, 2003. The
estimation and detection of stimuli by sensory neurons is affected by
factors that govern a transition from tonic to burst mode and the
frequency chracteristics of burst output. Pyramidal cells in the
electrosensory lobe of weakly electric fish generate spike bursts for
the purpose of stimulus detection. Spike bursts are generated during
repetitive discharge when a frequency-dependent broadening of dendritic
spikes increases current flow from dendrite to soma to potentiate a
somatic depolarizing afterpotential (DAP). The DAP eventually triggers
a somatic spike doublet with an interspike interval that falls inside
the dendritic refractory period, blocking spike backpropagiation and
the DAP. Repetition of this process gives rise to a rhythmic dendritic
spike failure, termed conditional backpropagation, that converts cell
output from tonic to burst discharge. Through in vitro
recordings and compartmental modeling we show that burst frequency is
regulated by the rate of DAP potentiation during a burst, which
determines the time required to discharge the spike doublet
that blocks backpropagation. DAP potentiation is maginfied through a
postitve feedback process when an increase in dendritic spike duration
activates persistent sodium current (INaP).
INaP further promotes a slow depolarization that
induces a shift from tonic to burst discharge over time. The results
are consistent with a dynamical systems analysis that shows that the threshold separating tonic and burst discharge can be represented as a
saddle-node bifurcation. The interaction between dendritic K+ current and INaP provides a
physiological explanation for a variable time scale of bursting
dynamics characteristic of such a bifurcation.
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