When Geoffrey Murphy talks about plastic structures, he’s not talking about the same thing Mr. McGuire referred to in “The Graduate.” To Murphy, associate professor of molecular and integrative physiology at the Medical School, plasticity refers to the brain’s ability to change as we learn.
Murphy’s lab, in collaboration with the U-M Neurodevelopment and Regeneration Laboratory run by Dr. Jack Parent, recently showed how the plasticity of the brain allowed mice to restore critical functions related to learning and memory after the scientists suppressed the animals’ ability to make certain new brain cells.
The findings, published online in the Proceedings of the National Academy of Sciences, bring scientists one step closer to isolating the mechanisms by which the brain compensates for disruptions and reroutes neural functioning. Ultimately, that could lead to treatments for human cognitive impairments caused by disease and aging.
“It’s amazing how the brain is capable of reorganizing itself in this manner,” says Murphy, co-senior author of the study and researcher at U-M’s Molecular and Behavioral Neuroscience Institute. “Right now, we’re still figuring out exactly how the brain accomplishes all this at the molecular level, but it’s sort of comforting to know that our brains are keeping track of all of this for us.”
In previous research, the scientists had found that using radiation or genetic manipulation to restrict cell division in the hippocampuses of mice resulted in reduced functioning in a cellular mechanism important to memory formation known as long-term potentiation.
But in this study, the researchers demonstrated that the disruption is temporary, and within six weeks the mouse brains were able to compensate for the disruption and restore plasticity, says Parent, the study’s other senior author, a researcher with the VA Ann Arbor Healthcare System and associate professor of neurology at the Medical School.
After halting the ongoing growth of key brain cells in adult mice, the researchers found the brain circuitry compensated for the disruption by enabling existing neurons to be more active. The existing neurons also had longer life spans than when new cells were continuously being made.
Additional authors are Benjamin Singer, Amy Gamelli, Cynthia Fuller and Stephanie J. Temme, all of U-M.
