Working with mice reared in a low-oxygen environment from three to 11 days after birth, the researchers found that about 30 percent of the cortical neurons were lost from the injury. But this damage was transient. The lost cortical neuron number, volume and brain weight were all reversed during the recovery period.
The findings suggest that newly generated neurons and glial cells migrate in the cerebral cortex of the infant mouse brain. This may play a significant role in repairing neuronal losses after neonatal injury, according to lead author Flora Vaccarino, M.D., associate professor in the Yale Child Study Center and in neurobiology at Yale.
Chronic perinatal hypoxia represents a major risk factor for cognitive handicap and attention deficit hyperactivity disorder. Yet clinical data suggests that the incidence of disability decreases over childhood and adolescence. Vaccarino and her team tested for a probable mechanism of recovery.
"Remarkably, even without injury, the juvenile mouse cortex is able to generate new neurons," said Vaccarino. "This suggests that the mammalian brain is far more plastic than previously thought and thus may be able to recover from serious brain injuries."
Other authors on the study included Devon M. Fagel1, Yosif Ganat, John Silbereis, Timothy Ebbitt, William Stewart, Heping Zhang and Laura R. Ment, M.D.
The study was funded by the National Institute of Neurological Disorders and Stroke.
Citation: Experimental Neurology, (Article In Press).
Journal
Experimental Neurology