Like paramedics waiting for an emergency, cells that help heal injuries are stationed around the brain. Tong et al. have intercepted the signal that dispatches these cells to their posts.
NG2 cells spawn the oligodendrocytes that produce insulating myelin for the central nervous system. During development, NG2 cells arise in the brain's ventricular zone and then fan out to other parts of the organ. They remain in position, presumably providing a reserve that can replace lost and damaged oligodendrocytes after an injury. The unanswered question is what triggers their move.
Tong et al. connected the cells' migration to their electrophysiology. Like neurons, NG2 cells depolarize after stimulation, allowing in a flood of sodium ions—although they can't muster a full-fledged action potential. After this surge of sodium ions, a calcium influx follows as sodium–calcium exchanger proteins kick into gear. The researchers found that the neurotransmitter GABA, released from neighboring neurons, spurs the sodium and calcium inflow into NG2 cells. Reducing the levels of sodium channels or exchanger proteins with RNAi stymied GABA's effect on calcium.
The team also gauged NG2 cell movement in culture and in brain slices from newborn rats. The cells traveled toward sources of GABA. By inducing sodium and calcium inflow, the findings suggest, GABA prods NG2 cells to disperse through the brain. This pathway differs from the pathway that spurs neuron migration, which involves calcium channels.