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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: J Comput Neurosci. 2015 May 1;39(1):17–28. doi: 10.1007/s10827-015-0562-8

Figure 3.

Figure 3

Transition from phase 1 to phase 2 AD. (A) Increased axon diameter results in longer lasting AD. To isolate phase 1 AD, phase 2 AD was prevented by removing gNaP from the soma for these simulations. Note that since a single evoked spike is sufficient to trigger phase 1 AD based on the neuroma gNaP of 1.9 mS/cm2, absence of phase 1 AD in the left panel indicates that AD fails without becoming manifest, which is mechanistically distinct from AD not being triggered. (B) Triggering of Phase 2 AD depends on number of spikes comprising phase 1 AD. For these simulations, gNaP was re-inserted in the soma (0.19 mS/cm2). Panel a shows failure to trigger phase 2 AD. Panels b and c show that phase 1 AD comprises the same number of spikes regardless of whether it is followed by phase 2 AD (cf corresponding panels in A), indicating that phase 2 AD starts only after phase 1 AD ends. (C) When somatic gNaP was increased to 0.28 mS/cm2, a spike (marked by *) originated in the soma before the end of phase 1 AD, as evidenced by the somatic spike preceding the propagated spike recorded at the node midway between the soma and neuroma. This example nicely illustrates how two sites, each capable of initiating spikes, compete to serve as pacemaker for the neuron.