Dissociation between sustained single-neuron spiking β-rhythmicity and transient β-LFP oscillations in primate motor cortex

Some of my thesis work has just been published!

Rule et al. 2017 explores the neurophysiology of beta (β) oscillations in primates, especially how single-neuron activity relates to population activity reflected in local field potentials (a.k.a. "brain waves").

β (~20 Hz) oscillations occur in frontal cortex. We've known about them for about a century, but still don't understand how they work or what they do. β-wave activity is related to "holding steady", so to speak.

β is dysregulated in Parkinson's, in which movements are slowed or stopped. β is also reduced relative to slow-wave activity (θ) in ADHD, a disorder associated with motor restlessness and hyperactivity.

I looked at β oscillations during movement preparation, where β seems to play a role in stabilizing a planned movement. We found that single neurons had very little relationship to the β-LFP brain waves. However! This appears to be for a good reason: the firing frequencies of neurons store information about the upcoming movement, and so are diverse and cannot lock to a single frequency.

Anyone who's played in an orchestra knows that when notes are just slightly out of tune, you get interference patterns called beats. The same thing is happening in the brain, where many neurons firing at slightly different "pitches" cause β-LFP fluctuations, even though the underlying neural activity is constant.

This result provides a new explanation for how β-waves can appear as "transients" during motor steady-state: the fluctuations are cased by "beating", rather than changes in the β activity in the individual neurons. This differs from the prevailing theory for the origin of β transients in more posterior brain regions.

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