However, the nature of this internal feedback pathway and whether it has any impact on movement have not been clear. "If PNs were indeed sending copies of outgoing motor commands to the brain, they could provide a conveniently rapid means of adjusting ongoing movements when things go awry," said Eiman Azim, PhD, a postdoctoral fellow in Dr. Jessell's lab and lead author of the first paper. "But without a way to selectively target the copy function of PNs, there was no way to test this theory."
The CUMC team, in collaboration with Bror Alstermark, PhD, a professor in integrative medical biology at Ume University in Sweden, overcame this technical barrier by developing a genetic method for accessing and eliminating PNs in mice, abolishing both motor-directed and copy signals sent by the neurons. When the researchers quantified the limb movements of the PN-deprived mice in three dimensions as they reached for food pellets, they found that the mice's ability to reach for the target accurately was badly compromised. "Basically, their movements were uncoordinated," said Dr. Azim. "The PN-deprived mice consistently over- or under-reached."
But with both PN output signals gone, the precise role of the PN copy signal remained unclear. The researchers then turned to optogeneticsthe use of light to control neuronal activity. They selectively activated the copy axonal branch alone, decalibrating this copy signal from the version sent to motor neurons. With the copy signal altered, the an
|Contact: Karin Eskenazi|
Columbia University Medical Center