Brain plasticity

From Yenra

Researchers have long sought a factor that can trigger the brain's ability to learn – and perhaps recapture the sponge-like quality of childhood. In the August 8, 2008 issue of the journal Cell, neuroscientists at Children's Hospital Boston report that they've identified such a factor: a protein called Otx 2.

Otx2 helps a key type of cell in the cortex to mature, initiating a critical period -- a window of heightened brain plasticity, when the brain can readily make new connections.

The work was done in a mouse model of the visual system, a classic model for understanding how the brain sets up its wiring in response to input from the outside world. But similar factors from the auditory, olfactory and other sensory systems may help time critical periods. Timing is important, because the brain needs to rewire itself at the right moment -- when it's getting the optimal sensory input.

Being able to control the timing of critical periods in different parts of the brain could possibly ameliorate developmental disorders such as autism, in which researchers believe critical periods may be inappropriately accelerated or delayed. Retriggering a critical period might also help people learn more readily after childhood – acquiring a new language, developing musical abilities or recovering from stroke or brain injury, for example.

Researchers found that the brain cells that switch on critical periods in the visual system (parvalbumin cells) don't actually make Otx2 themselves. Instead, Otx2 is sent by the retina.

It was previously known that when parvalbumin cells mature, they set up inhibitory circuits in the cortex, balancing the existing excitatory circuits. Now it is clear that setting up inhibitory circuits is key in launching critical periods.

In the current study, Hensch and colleagues demonstrated that when mice are reared in the dark, thus getting no visual input, Otx2 remains in the retina. Only when the mice received full visual input did Otx2 begin to appear in the cortex, and only then did parvalbumin cells start to mature.

In other experiments, the researchers injected Otx2 directly into the cortex. The parvalbumin cells matured, even when the mice were kept in the dark. Finally, when Otx2 synthesis was blocked in the eye, parvalbumin cell functions failed to mature.

Otx2 has an unusual derivation: it is originally produced during embryonic development; without it, mice don't develop heads. Production then stops, but some days after birth, it reappears in parvalbumin cells.