Stressed neurons ran out of energy and became silent but could still survive for hours, potentially giving physicians time to intervene, unless depolarization follows. Without sufficient oxygen and energy, internal pumps that ensure proper polarity by removing sodium and pulling potassium into neurons, can stop working and dramatically accelerate brain-cell death.
"Like the plus and minus ends of a battery, neurons must have a negative charge inside and a positive charge outside to fire," Kirov said. Firing enables communication, including the release of chemical messengers called neurotransmitters.
"If you have six hours to save tissue when you have just lost part of your blood flow, with this spreading depolarization, you lose tissue within minutes," he said.
While common in head trauma, spreading depolarization would not typically occur in less-traumatic injuries, like his model. His model was chemically induced to reveal more about how this collateral damage occurs and whether neurons could still be saved. Interestingly, researchers found that without the initial injury, brain cells completely recovered after re-polarization but only partially recovered in the injury model.
While very brief episodes of depolarization occur as part of the healthy firing of neurons, spreading depolarization exacerbates the initial traumatic brain injury in more than half of patients and results in poor prognosis, previous research has shown. However, a 2011 review in the journal Nature Medicine indicated that short-lived waves can actually protect surrounding brain tissue. Kirov and his colleagues wrote that more study is needed to determine when to intervene.
One of Kirov's many next steps is exploring the controversy about whether astrocytes' swelling in response to physical trauma is a protective response or puts the cells in destruct mode. He also wants to explore better ways to prote
|Contact: Toni Baker|
Medical College of Georgia at Georgia Regents University