Finding an accurate explanation of beta oscillations might not only help explain why the brain's perceptual circuits are wired the way they are, but could also provide doctors with a rational means for improving deep-brain stimulation treatments for Parkinson's disease and maybe obsessive compulsive disorder where they apply electrical current to parts of the brain that Moore and Jones suspect of relaying beta signals.
"You'd have a mechanistic understanding of why that change [from stimulation] created that change in the circuit," Jones said.
One day at lunch ...
The two launched their discussion a few years ago in the cafeteria at Massachusetts General Hospital when Moore, then at the Massachusetts Institute of Technology, and Jones, then at the hospital, realized that the circuits he studied in the physical brain were the very ones she modeled in a computer. In particular they shared an interest in a touch-perception circuit, technically known as a "thalamocortical circuit in the somatosensory system."
After they began to collaborate, Jones shared that her computational model suggested human data on beta oscillations could best be produced by a delivering a two-signal trigger to neurons in the circuit. One signal comes in at the far end of a neuron where the cell's long branches, or dendrites, extend out. The other, she said, would have to come in at the base of that tree-like structure, where the dendrite extends out from the cell.
In neuroscience orthodoxy, no one has ever said that beta oscillations are triggered by such a combination of two signals but then, orthodoxy has so far failed to explain beta oscillations.
Moore had his doubts but experiments began to show indeed that Jones's model, which simulated a circuit of about 300 cells of about five types, predicted what he could observe in real animal brains. In 2009 and 2010 the two
|Contact: David Orenstein|