Picture yourself driving home. Half way there, you find a huge tree in the middle of the road, blocking your normal route. Rather than abandoning hope, you turn around and go home by another way.
When our brain regains function after one region is damaged, this effectively is what it is doing. Though this plasticity of the brain has been observed for many years, how this happens is just starting to be understood.
In a new study life scientists from University of California, Los Angeles, and the Garvan Institute of Medical Research in Australia report one mechanism of brain compensation–recruitment of alternate circuits. These pathways, somewhat surprisingly, do not need to be near the damaged site.
“Most views of compensation following tissue loss (stroke for example) think of compensation occurring in adjacent tissue,” write the authors. “A unique finding here is that compensation can occur in regions that are not directly proximal to the site of injury.”
The hippocampus, a small seahorse-shaped structure deep in the brain, is the brain’s bedrock of learning and memory formation. It can be damaged by a lack of oxygen or a stroke, and its dysfunction is key in Alzheimer’s disease
To test the brain’s rewiring capacity, Moriel Zelikowsky and her colleagues taught lab rats to fear a tone, through conditioning with electrical shocks. Damage to the hippocampus removed this fear and slowed their ability to form memories post-injury. The animals were still able to learn, however, by bringing a section of the brain known for storing long-term memories, into action.
To find this, Zelikowsky traced early gene expression in the brain following injury to the hippocampus. She found dramatic rearrangement of cells in the frontal cortex, specifically in the infralimbic and prelimbic regions of the medial prefrontal cortex (mPFC).
The researchers believe the mPFC is playing a more general role in memory and context-sensitive learning, rather than the specific role it has been assigned in the past, of exciting and inhibiting fear.
Researchers hope this understanding will eventually direct them toward treatments for patients suffering degeneration or memory loss after a brain injury. Many have tried to simulate repair within the hippocampus, for instance, but these findings open new possible targets.
“Interestingly, previous studies had shown that these prefrontal cortex regions also light up in the brains of Alzheimer’s patients, suggesting that similar compensatory circuits develop in people,” co-author Bryce Vissel told UCLA.
“While it’s probable that the brains of
Alzheimer’s sufferers are already compensating for damage, this discovery has significant potential for extending that compensation and improving the lives of many.”