The time window for the brain to develop optimal connections based on learning and experience is relatively short-lived, occurring prior to adulthood. But this neuroplasticity can be restarted in the visual cortex of adult mice, according to the results of a study published in Science Translational Medicine. Directly inhibiting the activity of a protein, known to put a brake on neural plasticity early during post-natal development, resulted in growth of new neural synapses and restored eyesight in adult animals with so-called “lazy eye.”
“There is a lot of interest in the ‘critical period’ of development when the brain is plastic and undergoes a lot of changes and learning,” said Christiaan Levelt, who studies the biology of visual plasticity at the Netherlands Institute for Neuroscience in Amsterdam and was not involved in this work. “This study shows that, in an adult animal, you can re-open this critical period window and get enhanced plasticity.”
“At its heart, this is about understanding why it gets harder to learn new things as we get older and whether this is something that we can reverse if we knew the right molecules to target, by either adding them back or by suppressing them,” said study author David Bochner, who just completed his PhD research at Stanford University.
Bochner, his Stanford advisor Carla Shatz, and their colleagues took the latter approach. Shatz’s laboratory had previously discovered that the Paired-immunoglobulin–like receptor B (PirB) protein, expressed in a subset of neurons in the brain, works to halt the plasticity of the visual cortex: a knockout PirB mouse has better plasticity in this part of the brain throughout its life. In the current study, the researchers disrupted PirB function—either genetically or biochemically—and saw new, functional synapses form, demonstrating that even when PirB is inhibited in a short, one-week time frame, new neuron connections—and recovery from lazy eye—is possible in an adult mouse.
Read full, original article: Turning Back the Brain’s Clock
