Compare passive spread with thresholded signal regeneration
A local membrane voltage change spreads through electrical properties of the membrane and cytoplasm, but passive spread diminishes with distance. An action potential is regenerated through voltage-dependent channel activity rather than being a single unchanged charge packet traveling intact along the axon. The distinction explains why a passive signal and a propagated spike require different models.
Learning outcome: Compare λ=2 and λ=1 at node spacing 1. Retain first arriving amplitude, successful-node count and final passive versus regenerated outputs. Explain which parts of an actual action potential are absent.
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Identify neural and endocrine pathways, then separate electrochemical equilibrium, signal regeneration, synaptic conductance, receptor binding and secretion–clearance feedback using original bounded evidence.
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At λ=2 and node spacing 1, first arrival is 10e^(−0.5)≈6.065, above 4, so each node regenerates to 10. Pure passive amplitude at distance 4 is 10e^(−2)≈1.353. Both traces begin at 10 but follow different mechanisms.
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Can a small first-node input change cause a large downstream difference under a regeneration threshold?
Experiment
Compare λ=2 and λ=1 at node spacing 1. Retain first arriving amplitude, successful-node count and final passive versus regenerated outputs. Explain which parts of an actual action potential are absent.
Compare passive attenuation with thresholded node regeneration
Worked teaching model · synthetic values · Original initial signal 10; passive amplitude 10exp(−distance/λ). At each of four nodes, arriving amplitude at least 4 resets to 10; below 4 propagation fails permanently. Ideal threshold rule illustrates regeneration, not a biophysical action-potential waveform or stimulation protocol.
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Regeneration maintains a signal only when each next node receives sufficient local input.
Myelin changes membrane electrical properties and allows saltatory propagation between excitable nodes. This ideal threshold reset is not a detailed ion-channel waveform, refractory model or real demyelination diagnosis.
Solid: passive amplitude.Dashed: regenerated node output. Lines connect sampled model states; they do not supply unmodeled continuous physiology.
| Distance | Primary value | Comparison |
|---|---|---|
| 0 | 10 | 10 |
| 1 | 6.065307 | 10 |
| 2 | 3.678794 | 10 |
| 3 | 2.231302 | 10 |
| 4 | 1.353353 | 10 |
| Quantity | Value | Unit |
|---|---|---|
| First-node arriving amplitude | 6.065307 | signal units |
| Nodes successfully regenerated | 4 | nodes |
| Passive amplitude at fourth node | 1.353353 | signal units |
| Regenerated output at fourth node | 10 | signal units |
Original schematic mechanisms and invented parameters. No personal testing, electrical stimulation, hormone manipulation or clinical interpretation.
Regeneration maintains a signal only when each next node receives sufficient local input.
Myelin changes membrane electrical properties and allows saltatory propagation between excitable nodes. This ideal threshold reset is not a detailed ion-channel waveform, refractory model or real demyelination diagnosis.
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At λ=1 and spacing 1, does the first node regenerate, and what is the fourth-node passive amplitude?
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