Evidence that alpha blocking is due to increases in system-level oscillatory damping not neuronal population desynchronisation
David T. J. Liley, Suresh Muthukumaraswamy
NeuroImage November 29, 2019 DOI: 10.1016/j.neuroimage.2019.116408 via OpenAlex
Summary
The reduction in alpha-band brain wave power when people open their eyes is explained by increased damping of oscillatory activity, not by changes in neuronal population synchrony as commonly believed. Using time series modeling of EEG data, the authors found that the NMDA antagonist ketamine modifies these damping changes through glutamatergic neurotransmission. The results challenge the prevailing view that thalamus and neuronal population synchronization drive alpha rhythm generation and modulation, suggesting instead that physiological damping dynamics play a key role.
Study at a glance
| Characteristics | Observational study Peer reviewed |
|---|---|
| Intervention | Ketamine |
| Keywords | Neuroscience Glutamatergic Population Alpha finance Nmda receptor |
| Citations | 18 |
| Key finding | The reduction in alpha-band power between eyes-closed and eyes-open states is due to increased damping of alpha-band oscillatory activity, not changes in neuronal population synchrony. |
Abstract
The attenuation of the alpha rhythm following eyes-opening (alpha blocking) is among the most robust features of the human electroencephalogram with the prevailing view being that it is caused by changes in neuronal population synchrony. To further study the basis for this phenomenon we use theoretically motivated fixed-order Auto-Regressive Moving-Average (ARMA) time series modelling to study the oscillatory dynamics of spontaneous alpha-band electroencephalographic activity in eyes-open and eyes-closed conditions and its modulation by the NMDA antagonist ketamine. We find that the reduction in alpha-band power between eyes-closed and eyes-open states is explicable in terms of an increase in the damping of stochastically perturbed alpha-band relaxation oscillatory activity. These changes in damping are putatively modified by the antagonism of NMDA-mediated glutamatergic neurotransmission but are not directly driven by changes in input to cortex nor by reductions in the phase synchronisation of populations of near identical oscillators. These results not only provide a direct challenge to the dominant view of the role that thalamus and neuronal population de-/synchronisation have in the genesis and modulation of alpha electro-/magnetoencephalographic activity but also suggest potentially important physiological determinants underlying its dynamical control and regulation.