Traumatic brain injury (TBI) incidences have been seemingly increasing over the years among military personnel and sports persons. Experts from the UT Southwestern Medical Center have now laid hands on the probable way brain’s memory center repairs itself after severe trauma. The unfolded process can supposedly explain why it is harder to bounce back after multiple head injuries.
It was noted that mice that were unable to create new nerve cells in the brain’s memory area, hippocampus following brain trauma purportedly faced significant learning and memory problems. The hippocampus possibly contains a well of neural stem cells that become neurons in response to injury. These stem cells have to allegedly grow into functioning nerve cells for repairing the damage.
“Traumatic brain injury (TBI) has received a lot of attention recently because of the recognition that both military personnel and football players suffer from debilitating brain injuries. We have discovered that neural stem cells in the brain’s memory area become activated by injury and remodel the area with newly generated nerve cells. We also found that the activation of these stem cells is required for recovery,” said senior investigator, Dr. Steven G. Kernie,associate professor of pediatrics and developmental biology at UT Southwestern.
During the research, scientists developed unique transgenic mice that were incapable of creating hippocampal neurons when exposed to a usually harmless chemical called ganciclovir soon after brain injury. Two groups of these transgenic mice received either sham surgery or a controlled cortical injury (CCI) to mimic the diffuse damage of a moderate to severe head injury. And the other two groups were exposed to ganciclovir.
On completion of a month, mice were subjected to a learning task named the Morris water maze. In this task, the mice had to find a white platform hidden in a white pool of water. No group-noteworthy differences in swim speed were registered on the first day of learning the task. So no presence of motor impairment appeared in the test mice. However, in the next 10 days, the test group allegedly spent more time swimming along the edges of the tank, and they traveled longer distances to reach the platform.
“This suggests that injured mice who lack new nerve cells fail to progress to a more efficient spatial strategy to find the hidden platform. We interpret this result as a mild but statistically significant learning deficit,” Dr. Kernie said.
The mice were allowed to rest for a day and the platform was removed. Mice were retested to see how well they remembered about the platform’s location. In comparison to controls, CCI mice reportedly displayed no preference for the platform’s previous location or even for the target quadrant of the pool where the platform had been. CCI mice with intact nerve cell generation presumably had an intermediate response to the water maze and non-CCI mice with intact nerve cell generation had the best response. It was concluded that neurogenesis may be vital for learning after TBI.
The research was published in The Journal of Neuroscience.