This ModelDB entry contains a morphologically detailed Layer 2/3 pyramidal neuron model used to identify the biophysical mechanism underlying reduced excitability in callosal-receiving neurons (CRNs). By varying D-type (Kv1.1/1.2) and M-type (Kv7.2/7.3) K conductances, the model shows that elevated Kv1 density alone reproduces the downward-shifted CRN f–I curve. Dendritic Ca electrogenesis remains largely unchanged across conditions. Model prediction: CRN excitability—and thus binocular integration strength—can be bidirectionally tuned by modest changes in Kv1 channel density at the axon initial segment. Increasing Kv1 suppresses firing gain and raises spike threshold, whereas reducing it restores a non-CRN–like high-gain response. This identifies Kv1 channels as the primary intrinsic regulator of non-reciprocal callosal communication.
Experimental motivation: Experiments in mouse binocular visual cortex showed that callosal-receiving neurons (CRNs) fire less robustly than non-CRNs despite having similar morphology and comparable thalamic input. Transcriptomic and electrophysiological data identified elevated Kv1 (KCNA2) expression in CRNs, suggesting that intrinsic membrane mechanisms—rather than synaptic or structural differences—drive their reduced excitability. Current-clamp recordings confirmed a downward-shifted CRN f–I curve, and voltage-clamp data highlighted a prominent contribution from low-threshold potassium currents. These findings motivated the development of a morphologically detailed, channel-explicit NEURON model to test whether changes in Kv1/Kv7 conductance are sufficient to explain CRN firing behavior and to generate predictions about how intrinsic conductances regulate interhemispheric communication.
Model Type: Neuron or other electrically excitable cell
Region(s) or Organism(s): Visual cortex
Cell Type(s): Hodgkin-Huxley neuron
Currents: I A; I Potassium; I Sodium; IK Skca; I_AHP; I_KD
Receptors:
Genes: Kv1.1 KCNA1; Kv1.2 KCNA2
Transmitters:
Model Concept(s): Action Potentials
Simulation Environment: NEURON
References: