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The Journal of Neuroscience, January 1, 2001, 21(1):125-135

The Contribution of Dendritic Kv3 K⁺ Channels to Burst Threshold in a Sensory Neuron

Asim J. Rashid¹, Ezequiel Morales², Ray W. Turner², and Robert J. Dunn¹

¹ Departments of Neurology and Biology, McGill University, and Center for Research in Neuroscience, Montreal General Hospital, Montreal, Quebec, Canada H3G 1A4, and ² Neuroscience Research Group, University of Calgary, Calgary, Alberta, Canada T2N 4N1

Voltage-gated ion channels localized to dendritic membranes can shape signal processing in central neurons. This study describes the distribution and functional role of a high voltage-activating K⁺ channel in the electrosensory lobe (ELL) of an apteronotid weakly electric fish. We identify a homolog of the Kv3.3 K⁺ channel, AptKv3.3, that exhibits a high density of mRNA expression and immunolabel that is distributed over the entire soma-dendritic axis of ELL pyramidal cells. The kinetics and pharmacology of native K⁺ channels recorded in pyramidal cell somata and apical dendrites match those of AptKv3.3 channels expressed in a heterologous expression system. The functional role of AptKv3.3 channels was assessed using focal drug ejections in somatic and dendritic regions of an in vitro slice preparation. Local blockade of AptKv3.3 channels slows the repolarization of spikes in pyramidal cell somata as well as spikes backpropagating into apical dendrites. The resulting increase in dendritic spike duration lowers the threshold for a -frequency burst discharge that is driven by inward current associated with backpropagating dendritic spikes. Thus, dendritic AptKv3.3 K⁺ channels influence the threshold for a form of burst discharge that has an established role in feature extraction of sensory input.

Key words: potassium channel; Kv3; dendritic spike; action potential; backpropagation; oscillatory discharge; repolarization; DAP; electrosensory

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Copyright © 2001 Society for Neuroscience  0270-6474/01/211125-11$05.00/0

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