The brain never really loses its ability to act young—it just uses a brain receptor to turn that ability off, a new study suggests.

In a young person (or a young mouse, in the case of this study), brain circuits are more plastic—they're highly moldable, reorganizing with ease and making new connections to learn new tasks. As we get older, our brains become hardened, which is why it's harder and takes longer to learn new skills when you're older.

Figuring out how to keep brains more plastic could improve memory and learning in adults, and it could help people suffering from stroke and dementia. Researchers took another step toward that breakthrough with this study today in Science Translational Medicine.

Probing Plasticity

David Bochner, a postdoctoral researcher at Stanford, and neurobiology professor Carla Shatz wanted to study a receptor called paired immunoglobulin-like receptor B (PirB). Earlier research had found that mice lacking this receptor recovered better after strokes and didn't demonstrate memory problems associated with a mouse version of Alzheimer's. However, it was unclear whether and how the receptor was associated with brain plasticity.

To investigate these questions, the team worked with mice that had a lazy eye. Why? The way that the brain works with the eyes can be an amazing demonstration of neuroplasticity. Our brains have two sets of neurons that correspond to each eye, but if one eye isn't working correctly at a very young age, then these channels can reorganize to favor the working eye. This can lead to abnormal brain wiring getting "locked in." Younger animals are better able to recover from this.

The researchers removed one eye from their subject mice, some of which had been bred or modified to lack PirB, and some of which had not. They then measured the mice's ability to adjust to the loss of sight. Later, they used a chemical to suppress PirB function in the brain. They also ran these tests on mice who had one eye blocked instead of removed.

Both the genetically modified mice and the drug-treated mice, whose PirB was blocked, demonstrated greater plasticity. This means they could adjust quickly to the loss of vision in one eye, just as they would if they were young. Importantly, the scientists saw this effect not only during the "critical period"—defined as the time in which the eye-connected neurons can be modified—but also in adulthood.

This shows that PirB is definitely involved in plasticity, the researchers say. "It just allows the normal mechanisms of neural plasticity to naturally increase," he says. "So instead of turbo-charging the system, or whacking it with a sledgehammer, we're strategically loosening a few parts here, adding some oil there, and letting the system run better under its own power."

What's the Point?

Bochner likens PirB to a braking system. But why this brake exists in the first place remains an open question. What would be the evolutionary benefit of shutting down plasticity?

Bochner says there may be some advantages to being hard-wired.

"You want to be able to reliably move your muscles when you want, and you also don't want your vision to change every time you wink," he says. "Setting a reasonably high threshold for inducing plastic change in the brain could be helpful to keep things fast, hard-wired, and reliable when you need them."

But, he adds, the trade-off is that the brain might not be as flexible as you'd like, especially if you're a grown adult and you need to learn something new quickly or adjust to a major change or injury.

The mouse system these researchers studied doesn't work exactly like that found in humans, because our brains have more complicated pathways than mice. Humans have 5 different inhibitory immunoglobulin-like receptor molecules (LilrB), which are very similar to PirB. One of them, LilrB2, seems to be involved in patients with Alzheimer's disease. Figuring out which one of those molecules to target to improve plasticity would be an important next step, Bochner says.

Eventually, though, research on plasticity could improve our everyday brain function, enhancing our learning and memory processes throughout our lives.

"We don't know yet what would happen to learning and memory if we suppressed PirB, but it's possible that [plasticity would] be enhanced," Bochner says. "That's one of the things we're very excited to think about. What if a PirB-blocking pill could make you learn a new language faster, for example?"

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