Control of cardiac function and noise from a decaying power spectrum.

Abstract

Evidence is presented that adds to the debate surrounding the question: To what extent does neural control of cardiac output exploit noise? The transduction capability of cardiac afferent neurons, situated in and adjacent to the heart, is vital to feedback in control of cardiac function. An analysis of in situ cardiac afferent activity shows evidence of independent and exponentially distributed interspike intervals. An anatomical basis for such memoryless interspike intervals ultimately derives from the fact that each afferent neuron is associated with a field of sensory neurites, or bare nerve endings, that transduce local chemical and mechanical stimuli in a many-to-one fashion. As such, cardiac afferent neurons and their sensory neurite inputs are respectively modeled here by the Hodgkin-Huxley equations forced by "red" noise (decaying power spectrum) perturbing an otherwise constant subthreshold input. A variable barrier competition model is derived from these equations in order to address the question: How are noisy inputs being processed by sensory neurons to cause each spike? It is found that ion channels are responsible for significant input "whitening" (increased spectral power at higher frequency) through differentiation of the inputs. Such whitening is a means to distinguish low-frequency control signals from otherwise red noise fluctuations. Furthermore, spiking occurs when backward moving averages of the whitened inputs, over a window of the order of the sodium activation time scale, exceed an approximately constant barrier.