Abstract

Alpha blocking, a phenomenon where the alpha rhythm is reduced by attention to a visual, auditory, tactile or cognitive stimulus, is one of the most prominent features of human electroencephalography (EEG) signals. Here we identify a simple physiological mechanism by which opening of the eyes causes attenuation of the alpha rhythm. We fit a neural population model to EEG spectra from 82 subjects, each showing a different degree of alpha blocking upon opening of their eyes. Though it has been notoriously difficult to estimate parameters by fitting such models, we show how, by regularizing the differences in parameter estimates between eyes-closed and eyes-open states, we can reduce the uncertainties in these differences without significantly compromising fit quality. From this emerges a parsimonious explanation for the spectral differences between states: Changes to just a single parameter, pei, corresponding to the strength of a tonic excitatory input to the inhibitory cortical population, are sufficient to explain the reduction in alpha rhythm upon opening of the eyes. We detect this by comparing the shift in each model parameter between eyes-closed and eyes-open states. Whereas changes in most parameters are weak or negligible and do not scale with the degree of alpha attenuation across subjects, the change in pei increases monotonically with the degree of alpha blocking observed. These results indicate that opening of the eyes reduces alpha activity by increasing external input to the inhibitory cortical population.

Highlights

  • Alpha blocking is a classic feature of the human electroencephalogram (EEG)

  • Alpha blocking refers to the reduction in spontaneously-recorded occipital alpha band (8-13 Hz) power in response to opening of the eyes [3]

  • Distributions are estimated from the 100 best fit parameter sets for each subject. pei shows the most noticeable difference between its EC and EO distributions, with EO distributions drifting increasingly higher than their corresponding EC distributions as alpha blocking gets larger

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Summary

Introduction

Alpha blocking is a classic feature of the human electroencephalogram (EEG). Alpha blocking refers to the reduction in spontaneously-recorded occipital alpha band (8-13 Hz) power in response to opening of the eyes [3]. The mechanism associated with alpha blocking is typically considered separately from the mechanism associated with alpha wave generation. Whereas cortical alpha is often thought to be generated by feedforward and feedback interactions between the thalamus and overlying cortex [9,10,11,12], blocking is considered to arise from changes in the phase synchrony of populations of these near-identical cortico-thalamic alpha oscillators [13,14,15]. We show how alpha generation and blocking can be described self-consistently within a single neural population model for the cortex

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