20170126

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.

Optogenetic Stimulation Shifts the Excitability of Cerebral Cortex from Type I to Type II: Oscillation Onset and Wave Propagation

A new paper by Stewart Heitmann et al. could help us understand what happens when we stimulate cerebral cortex in primates using optogenetics. Modeling how the brain responds to stimulation is important for learning how to use this new technology to control neural activity.

Optogenetic stimulation elicits gamma (~50 Hz) oscillations, the amplitude of which grows with the intensity of light stimulation. However, traveling waves away from the stimulation site also emerge.

It's difficult to reconcile oscillatory and traveling-wave dynamics in neural field models, but Heitmann et al. arrive at a surprising and testable prediction: the observed effects can be explained by paradoxical recruitment of inhibition at low levels of stimulation, which changes cortex from a wave-propagating medium to an oscillator. (Excitation later overwhelms inhibition, giving rise to the observed gamma oscillations.)