Sigmoidal activation functions have been used in many models of neurons.
Some models allow this activation function to change, from flatter
sigmoids to steeper or vice versa. Is this biologically plausible?
This question can be elaborated a bit further. A sigmoidal activation
function approximates a plot of the output firing rate of a neuron( y-axis )
against the input activation of the neuron( x-axis).
When a sigmoid becomes steeper, the lower threshold increases, and
the upper threshold decreases. This would mean that our model neuron
starts firing at a higher threshold, but reaches its peak firing rate
(saturation) at a lower input activation. Is there any biological
evidence that this process happens in real neurons?
Change in activation function of a neuron can happen in many ways. One
of them would be migration of ion channels over the surface of the neuron.
The proportion of ion channels of various types in the axon hillock would
determine some of the triggering characteristics of the neuron. I have
come across evidence that ion channels migrate during synapse formation
at the neuromuscular junction( Kandel, Schwartz, Jessel - Principles of
Neuroscience ). However, do similar migration of ion channels happen in
the normal neurons? In particular, is there any evidence that migration
of ion channels is responsible for phenomena like habituation? Is there
evidence that the activation function changes when neurons are repeatedly
stimulated? Say with a tetanus?
Is there evidence that neurons during development change from more or less
linear and easily triggerable, to highly nonlinear as they mature?
Joseph Sirosh
