In deep brain stimulation (DBS) to treat movement disorders, a surgically implanted electrode delivers precise pulses into the brain’s movement centers. DBS is an effective treatment for Parkinson’s and other movement disorders, but exactly how it works is not well
understood. Because neurons communicate electrically, most scientists assume the procedure corrects or disrupts abnormal signaling among neurons.
Now Maiken Nedergaard and colleagues at the University of Rochester have found that electrical pulses stimulate the release of the chemical adenosine not from neurons but from astrocytes. These support cells do not transmit signals but play other roles in the brain—one of which is to produce adenosine throughout the day until levels are high enough to cause sleepiness.
Working with mouse brain tissue taken from the thalamus, a key movement center, Nedergaard’s team showed that DBS caused a marked increase of adenosine. In mice with an experimentally induced, Parkinson’s-like condition, infusions of adenosine alone into the
thalamus significantly reduced tremors. In addition, the investigators found that naturally occurring adenosine prevented the involuntary movements caused by excessive levels of electrical stimulation (which can be a side effect of treatment).
The findings, published in January in Nature Medicine, are the first to suggest a non-neuronal mode of action for DBS, Nedergaard says. “DBS is an invasive procedure,” she says. “Finding ways to target adenosine more immediately may help the procedure work better or even open up new, non-surgical treatments for Parkinson’s disease and other conditions.”