Spikes are usually initiated at the axon initial segment (AIS), the most excitable site of a neuron. Yet other regions of the neuron are also excitable. While there are many studies on somatic and dendritic excitability, axon excitability has yet to be thoroughly investigated in most neurons because the small size of the axon precludes intracellular recordings. Using a novel optogenetic approach, recent experiments from our lab have shown that axon spikes transiently in response to sustained depolarization. Although the optogenetic method has many advantages, it still has some limitations: first, light is not focused on one point, meaning stray light may hit other regions of the neuron; second, since voltage changes are recorded from the soma, the location of spike initiation must be inferred indirectly. These experimental limitations necessitated simulations to definitively interpret the experimental results. We built a multicompartment model of a CA1 pyramidal neuron with a detailed myelinated axon that reproduced our experimental data. The model confirmed the site of spike initiation based on the shape (kinkiness) of spikes recorded in the soma. Simulations also confirmed that even when targeting the axon for photostimulation, a small degree of stray light can hit the dendrites and evoke spikes in the AIS. The results ultimately confirm that the AIS spikes repetitively during sustained depolarization, consistent with analog to digital transduction of information, whereas the axon responds with transient spiking only during abrupt changes in depolarization. Simulations show that the stimulus the axon receives during spike propagation is a very intense and short depolarization, which is precisely the input to which it is tuned to respond.

Nooshin Abdollahi

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