Cortical neurons in the fluctuation driven regime can realize ultrafast population encoding. The underlying biophysical mechanisms, however, are not well understood. Reducing  action potential onset rapidness can impair the ultrafast population encoding, but it is not clear whether rapid action potential onset is sufficient for ultrafast population encoding. One hypothesis proposes that rapid action potential onset is caused by the  separation of the axon initial segment, that is the initiation site of action potentials, 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 a population of model neurons . We find that  the axonal initiation site position is not sufficient to generate an ultrafast response and reproduce the high bandwidth observed in cortical neuron populations . 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. By tuning the activation slope of the sodium current, we examined the impact of voltage sensitivity of sodium channels on population encoding. When high voltage sensitivity is introduced , the two empirically observed phenomena can be recovered.  By investigating varying soma sizes, we furthermore highlight the effect of neuron morphology on the linear response. Our results show that high onset rapidness of action potential initiation is not sufficient for  ultrafast response. In the light of recent experimental evidence about neural activity dependent repositioning of the axon initial segment and the resulting question about the functional properties of this phenomenon , our study predicts that , while it can lead to more rapid action potential onsets in the soma, it does not affect the linear response of a population of neurons.
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.
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the sharpness of the
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rapidness can impair the
can impair
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rapid
a sharp
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rapid
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electrotonic
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axon initial segment, that is the initiation
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potentials,
potential initiation
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a population of model neurons
model neurons with a defined initiation site
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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
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axonal initiation site position is not sufficient to generate an
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reproduce the high bandwidth
high bandwidth that is
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neuron populations
neurons
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By tuning the activation slope of the sodium current, we examined the impact of
When we increase the
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on population encoding. When high voltage sensitivity is introduced
at the initiation site
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We provide an explanation for the dissociation of sharp action potential onset and ultrafast response.
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high onset rapidness of action potential initiation
a sharp onset of action potentials
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the
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experimental evidence about neural activity dependent
reports of activity-dependent
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and the resulting question about the functional properties of this phenomenon
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, while it
a more distal initiation site
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more rapid action potential onsets in the soma,
an increased sharpness of the somatic waveform but