Input-dependent subcellular localization of spike initiation between soma and axon at cortical pyramidal neurons

Action potentials can be initiated at various subcellular compartments, such as axonal hillock, soma and dendrite. Mechanisms and physiological impacts for this relocation remain elusive, which may rely on input signal patterns and intrinsic properties in these subcellular compartments. We examined this hypothesis at the soma and axon of cortical pyramidal neurons by analyzing their spike capability and voltage-gated sodium channel dynamics in response to different input signals.

Electrophysiological recordings were simultaneously conducted at the somata and axons of identical pyramidal neurons in the cortical slices. The somata dominantly produced sequential spikes in response to long-time steady depolarization pulse, and the axons produced more spikes in response to fluctuated pulse. Compared with the axons, the somata possessed lower spike threshold and shorter refractory periods in response to long-time steady depolarization, and somatic voltage-gated sodium channels demonstrated less inactivation and easier reactivation in response to steady depolarization. Based on local VGSC dynamics, computational simulated spike initiation locations were consistent with those from the experiments. In terms of physiological impact, this input-dependent plasticity of spike initiation location made neuronal encoding to be efficient.

Long-time steady depolarization primarily induces somatic spikes and short-time pulses induce axonal spikes. The input signal patterns influence spike initiations at the axon or soma of cortical pyramidal neurons through modulating local voltage-gated sodium channel dynamics.