".. We carried out multi-site voltage-sensitive dye imaging of membrane potential transients from thin basal branches of prefrontal cortical pyramidal neurons before and after application of channel blockers. We found that backpropagating action potentials (bAPs) are predominantly controlled by voltage-gated sodium and A-type potassium channels. In contrast, pharmacologically blocking the delayed rectifier potassium, voltage-gated calcium or Ih, conductance had little effect on dendritic action potential propagation. Optically recorded bAP waveforms were quantified and multicompartmental modeling (NEURON) was used to link the observed behavior with the underlying biophysical properties. The best-fit model included a non-uniform sodium channel distribution with decreasing conductance with distance from the soma, together with a non-uniform (increasing) A-type potassium conductance. AP amplitudes decline with distance in this model, but to a lesser extent than previously thought. We used this model to explore the mechanisms underlying two sets of published data involving high frequency trains of action potentials, and the local generation of sodium spikelets. ..."
Model Type: Neuron or other electrically excitable cell
Region(s) or Organism(s): Neocortex
Cell Type(s): Neocortex L5/6 pyramidal GLU cell
Simulation Environment: NEURON
Implementer(s): Acker, Corey [acker at uchc.edu]
Acker CD, Antic SD. (2009). Quantitative assessment of the distributions of membrane conductances involved in action potential backpropagation along basal dendrites. Journal of neurophysiology. 101 [PubMed]