  Cortical neurons in the fluctuation driven regime can realize ultrafast
population encoding. The underlying biophysical mechanisms, however, are not
well understood. Reducing the sharpness of the action potential onset can
impair ultrafast population encoding, but it is not clear whether a sharp
action potential onset is sufficient for ultrafast population encoding. One
hypothesis proposes that the sharp action potential onset is caused by the
electrotonic separation of the site of action potential initiation from the
soma, and that this spatial separation also results in ultrafast population
encoding. Here we examined this hypothesis by studying the linear response
properties of model neurons with a defined initiation site. We find that
placing the initiation site at different axonal positions has only a weak
impact on the linear response function of the model. It fails to generate the
ultrafast response and high bandwidth that is observed in cortical neurons.
Furthermore, the high frequency regime of the linear response function of this
model is insensitive to correlation times of the input current contradicting
empirical evidence. When we increase the voltage sensitivity of sodium channels
at the initiation site, the two empirically observed phenomena can be
recovered. We provide an explanation for the dissociation of sharp action
potential onset and ultrafast response. By investigating varying soma sizes, we
furthermore highlight the effect of neuron morphology on the linear response.
Our results show that a sharp onset of action potentials is not sufficient for
the ultrafast response. In the light of recent reports of activity-dependent
repositioning of the axon initial segment, our study predicts that a more
distal initiation site can lead to an increased sharpness of the somatic
waveform but it does not affect the linear response of a population of neurons.
