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J Neurophysiol 89: 324-337, 2003; doi:10.1152/jn.00729.2002
0022-3077/03 $5.00
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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

Persistent Na+ Current Modifies Burst Discharge By Regulating Conditional Backpropagation of Dendritic Spikes

Brent Doiron,1 Liza Noonan,2 Neal Lemon,2 and Ray W. Turner2

 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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