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Conclusion

  1. The rapid rate of rise of spikes in the soma results largely from the initiation of the spike in the axon followed by back-propagation into the soma.
  2. The larger than expected variance in spike threshold in the soma results from the spike being initiated at a distal site (the axon), followed by back-propagation. In real neurons, the somatic and axonal compartments are exposed to somewhat different variations in membrane potential. This causes the spike in the soma to appear more variable in threshold than predicted by Hodgkin and Huxley models. In models, the variations in electrical properties of the soma and axonal initial segment has the same effect and suggests that this may also be true in real neurons.
  3. These properties (rapid somatic spike onset and spike threshold variability) are as expected by Hodgkin-Huxley models if the spike initiation properties of cortical neurons are taken into account.
  4. We conclude that there is no need to hypothesize the presence of exotic cooperative Na+ channel gating properties (Naundorf et al., Nature 440:1060) to explain these properties of action potential generation.