Slide 7

Figure 7. A Hodgkin-Huxley style model of spike generation by Pare, Lang and Destexhe demonstrate that the axon has a "smooth" onset, while the spike in the soma is "kinky". From Pare, Lang and Destexhe Neuroscience 84: 377 (1998).

Figure 5A. A Hodgkin-Huxley style model of spike generation by Baranauskas and Martina. Here the authors show that the "kink" in the somatic action potential of acutely dissociated pyramidal cells is modelled more accurately if the model axon has a higher density of Na+ than the soma and this "kink" can be improved by using m1, instead of m3, Na+ channel activation kinetics. Note the biphasic nature of spike generation in the models that have a higher density of Na+ in the axon than in the soma (J). From Baranauskas and Martina, J. Neuroscience 26: 671-684.

The results presented so far in this seminar indicate:

1. Spikes are typically initiated in the axon and back-propagate into the soma
2. This gives rise to a "biphasic" spike in the soma containing IS and SD components
   
3. Antidromic spikes exhibit a rapid rate of rise, a "kink", at spike initiation
   
4. A previous Hodgkin-Huxley model of spike generation in a full cortical neuron revealed a smooth rise in the axon and a "kink" in the soma
   
5. Two models have previously exhibited "kinks" in the somatic spikes when the axons are responsible for spike initiation
   

From these observations, we hypothesized that the rapid rate of rise of spikes in the soma and the variability of spike onset (as observed by Naundorf et al., 2006) both resulted from the initiation of spikes in the axon, followed by back propagation into the soma.

Here we make a simple model of spike generation in cortical neurons to explore this possibility.