Comparison of Langevin and Markov channel noise models for neuronal signal generation

Abstract

The stochastic opening and closing of voltage-gated ion channels produces noise in neurons. The effect of this noise on the neuronal performance has been modelled using either approximate or Langevin model, based on stochastic differential equations or an exact model, based on a Markov process model of channel gating. Yet whether the Langevin model accurately reproduces the channel noise produced by the Markov model remains unclear. Here we present a comparison between Langevin and Markov models of channel noise in neurons using single compartment Hodgkin-Huxley models containing either $N{a}^{+}$ and $K^{+}$, or only $K^{+}$ voltage-gated ion channels. The performance of the Langevin and Markov models was quantified over a range of stimulus statistics, membrane areas and channel numbers. We find that in comparison to the Markov model, the Langevin model underestimates the noise contributed by voltage-gated ion channels, overestimating information rates for both spiking and non-spiking membranes. Even with increasing numbers of channels the difference between the two models persists. This suggests that the Langevin model may not be suitable for accurately simulating channel noise in neurons, even in simulations with large numbers of ion channels.

References in corpus (3)

• Stochastic resonance as a collective property of ion channel assemblies
• Effect of channel block on the spiking activity of excitable membranes in a stochastic Hodgkin-Huxley model
• How Noise and Coupling Induce Bursting Action Potentials in Pancreatic beta-cells

Cited by in corpus (5)

• The what and where of adding channel noise to the Hodgkin-Huxley equations
• On stochastic differential equation models for ion channel noise in Hodgkin-Huxley neurons
• Channel noise induced stochastic facilitation in an auditory brainstem neuron model
• Fast and Accurate Langevin Simulations of Stochastic Hodgkin-Huxley Dynamics
• Effect of Channel Noise in Synchronization and Metabolic Energy Consumption in Unidirectionally Coupled Neurons: Drug Blocking of Sodium and Potassium Channels