Competitive exclusion between axons dependent on a single trophic substance: a mathematical analysis
Related Experiment Video
Updated: Nov 5, 2026

Examining Monosynaptic Connections in Drosophila Using Tetrodotoxin Resistant Sodium Channels
Published on: February 14, 2018
N Jeanprêtre1, P G Clarke, J P Gabriel
1Institut d'anatomie, Université de Lausanne, Switzerland.
Abstract:
A mathematical model is presented of competition between axons for a trophic substance, such as is believed to occur particularly during development. The model is biologically realistic. The growth-stimulating activity of the trophic molecules is assumed to result from their binding to high-affinity receptors on neurons and their axons, but the model also incorporates uptake by nonneuronal cells possessing only lower affinity receptors. Plausible and fairly general assumptions are made concerning the kinetics of binding and internalization and the effects on axonal growth. The model takes into account the possibility that trophic factor production may be regulated by the afferent axons or autoregulated. The variables specified are the "axonal vigor" of each axon, representing the ability of each axon to take up trophic molecules, and the concentration of trophic molecules in the extracellular space of the axonal target region. Of the several parameters introduced, the most important turns out to be the "zero vigor-growth parameter," which is defined as the concentration of trophic molecules that gives zero growth of the vigor of a given axon. By means of a Lyapunov function, it is shown that the system will approach asymptotically to a stable equilibrium characterized by the survival of only the axon whose zero-growth parameter is lowest. Or, if several axons share the same lowest zero-growth parameter, these will all survive. The model may be particularly relevant to the elimination of polyneuronal innervation from developing muscle fibers and from autonomic ganglion cells.
Related Concept Videos
The Role of Ion Channels in Neuronal Computation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
Pharmacodynamic Models: Linear Concentration–Effect Model
Propagation of Action Potentials
Neurons (nerve cells) have a resting membrane potential, with a slightly negative charge inside compared to outside. This is maintained by ion channels, such as sodium (Na+) and potassium (K+) channels, which control the flow of ions. When a stimulus, like a touch or a signal from another neuron, triggers the neuron, sodium channels open, allowing sodium ions to...
Pharmacodynamic Models: Emax Drug–Concentration Effect Model

