Myelin cells, which form an insulating layer around axons, secrete some of these inhibitory molecules. By experimenting with certain drugs that loosen myelin, Hensch and his collaborators found they could make the normally stable visual system of adult rodents become plastic again, allowing amblyopic rodents to recover. (However, the drug used in the study is toxic, making it unlikely to be a useful therapy.)
Given the usefulness of recapturing the neural facility of youth–the ability to quickly learn a new language, for example–it may seem odd that the brain would have evolved multiple mechanisms for preventing major rewiring in adults. But the capacity to easily overhaul neural circuits could have a downside, perhaps erasing memories. “You might lose the identity you’ve built,” says Hensch. “We want you to be able to keep what you know.”
To successfully co-opt the plasticity of youth, scientists will likely need to target treatments very precisely. “Maybe we can do a careful release of the critical period,” says Alison Doupe, a neuroscientist at the University of California, San Francisco, who was not involved in Hensch’s research. For example, “maybe you could turn on [plasticity] only when learning Russian.”
In addition to suggesting ways to enhance mental agility in old age, the findings may provide a new explanation for developmental disorders, such as autism.
Scientists have recently discovered that several strains of mice genetically engineered to mimic rare inherited forms of autism have an imbalance in levels of excitatory and inhibitory neural signals. Hensch’s previous research suggests that this kind of imbalance can throw the critical period out of whack. “Maybe different brain regions become plastic too early or too late [in autism],” says Hensch. That might also explain why disruptions to such different molecules can trigger similar symptoms, he says. “Maybe they have a common wiring problem.”
The researchers are now studying these imbalances in greater detail. For example, they found that mice from one of the strains, genetically engineered to show symptoms of autism, have too many neural connections in a specific part of the brain, although each connection is individually weak. “That could lead to too much variability,” says Hensch. “Maybe we can use that property to repair the circuit.”