When the brain’s primary learning center is damaged, new neural circuits arise to compensate for the lost function, a new study has found.
Researchers from the University of California-Los Angeles and Garvan Institute of Medical Research in Australia found that parts of the prefrontal cortex take over when the hippocampus — the brain’s key center of learning and memory formation — is disabled.
For the study, researchers Michael Fanselow, Ph.D. and Moriel Zelikowsky conducted laboratory experiments showing that rats were able to learn new tasks even after damage to the hippocampus. While the rats needed more training than they would have normally, they nonetheless learned from their experiences, said the researchers.
“I expect that the brain probably has to be trained through experience,” said Fanselow, who was the study’s senior author. “In this case, we gave animals a problem to solve.”
After discovering the rats could learn to solve problems, Zelikowsky, traveled to Australia to work with Dr. Bryce Vissel at the Garvan Institute. There, they analyzed the anatomy of the changes that had taken place in the rats’ brains.
Their analysis identified significant functional changes in two specific regions of the prefrontal cortex.
“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,” Vissel said.
“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.”
The hippocampus plays critical roles in processing, storing and recalling information, the researchers said. It is highly susceptible to damage through stroke or lack of oxygen and is “critically involved” in Alzheimer’s disease, according to Fanselow.
“Until now, we’ve been trying to figure out how to stimulate repair within the hippocampus,” he said. “Now we can see other structures stepping in and whole new brain circuits coming into being.”
Sub-regions in the prefrontal cortex compensated in different ways, with one sub-region — the infralimbic cortex — silencing its activity and another sub-region — the prelimbic cortex — increasing its activity, Zelikowsky said.
Complex behavior always involves multiple parts of the brain communicating with one another, with one region’s message affecting how another region will respond, Fanselow noted. These molecular changes produce our memories, feelings and actions.
“The brain is heavily interconnected — you can get from any neuron in the brain to any other neuron via about six synaptic connections,” he said. “So there are many alternate pathways the brain can use, but it normally doesn’t use them unless it’s forced to.
“Once we understand how the brain makes these decisions, then we’re in a position to encourage pathways to take over when they need to, especially in the case of brain damage.”
Behavior creates molecular changes in the brain, Fanselow said. “If we know the molecular changes we want to bring about, then we can try to facilitate those changes to occur through behavior and drug therapy. I think that’s the best alternative we have. Future treatments are not going to be all behavioral or all pharmacological, but a combination of both.”
The study was published in the journal Proceedings of the National Academy of Sciences.