Neuroscience 2005 Abstract
| Presentation Number: | 847.11 |
|---|---|
| Abstract Title: | Modulation of excitability by proximal axon KCNQ channels: a computational model. |
| Authors: |
Cranstoun, S. D.*1
; Pan, Z.2
; Cooper, E. C.2
1Bioengineering, Univ. of Pennsylvania, Philadelphia, PA 2Neurology, Univ. of Pennsylvania, Philadelphia, PA |
| Primary Theme and Topics |
Neural Excitability, Synapses, and Glia: Cellular Mechanisms - Ion Channels -- Potassium channels: Physiology |
| Secondary Theme and Topics | Techniques in Neuroscience<br />- Computation and Simulation |
| Session: |
847. Potassium Channels: M-Currents Poster |
| Presentation Time: | Wednesday, November 16, 2005 10:00 AM-11:00 AM |
| Location: | Washington Convention Center - Hall A-C, Board # J8 |
| Keywords: | POTASSIUM CHANNEL, AXON, MODEL, EXCITABILITY |
Heteromeric KCNQ2/KCNQ3 (Q2/Q3) channels underlie M-type voltage-gated K+ currents in sympathetic and hippocampal neurons. In brain, spinal cord, and sciatic nerve, a subpopulation of Q2 and Q3 proteins are concentrated at neuronal axon initial segments (AIS) and nodes of Ranvier, where they colocalize with the fast Na+ channels that initiate and propagate action potentials (APs). Physiological evidence indicates that KCNQ subunits underlie the slow, low-voltage-activated nodal K+ current, Ks (Schwarz JR et al., this meeting). Although it is believed that AP initiation occurs in the proximal axon, the exact locations, mechanisms, and modes of regulation of initiation are all incompletely understood. We have explored the potential function of KCNQ channels in the proximal axon, using computational modeling. We assembled a morphologically realistic CA1 pyramidal cell model, including dendrites, soma, and a myelinated axon, using NEURON. Somatodendritic compartments contained Na+ and K+ conductances at densities sufficient to propagate, but not initiate APs. Conductance densities at nodes of Ranvier were based on published data from peripheral axons. K+ conductances, with kinetics taken either from Q2/Q3, Ks or M-current recordings, were added at the AIS and/or first node, at densities estimated from somatic and nodal recording data. We determined the effects of axonal KCNQ channels on neuronal firing properties, when the site of AP initiation was either the AIS or first node. Irrespective of the AP initiation site, KCNQ-based currents localized to the AIS exerted strong effects, influencing firing thresholds, frequency and adaptation. When these K+ currents were eliminated from the AIS and included only at the nodes, they exerted much subtler effects. These simulations suggest a potential novel role for KCNQ channels in the AIS, and provide testable predictions for ongoing electrophysiological work.
Supported by NINDS R01 NS49119 and NICHD P30 HD26979 (ECC) and NSF-GSF, NIH T32-GM07517, NIH 1-R01-NS41811-03 and the Whitaker Foundation (SDC).
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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