Dr. Takao Hensch, a professor of neurology who was also a senior investigator on the study, has revealed that this finding results from a study on a mouse model of the visual system, which is often used to understand how the brain sets up its wiring in response to input from the outside world.
He and his colleagues say that Otx 2 works by helping a key type of cell in the cortex, parvalbumin cells, to mature.
During the study, the researcher observed that Otx2 remained in the mice's retina when they were reared in the dark, and got no visual input.
They say that it was only when the mice received full visual input did Otx2 begin to appear in the cortex, and only then did parvalbumin cells started to mature.
In another experiment, the researcher group injected Otx2 directly into the cortex, which caused the parvalbumin cells to mature even when the mice were kept in the dark.
However, when the researchers blocked Otx2 synthesis in the eye, parvalbumin cell functions failed to mature.
Background information in a research article published in the journal Cell suggests that Otx2 is originally produced during embryonic development, and that mice do not develop heads without it.
Its production then stops, and reappears in parvalbumin cells some days after birth.
"The nervous system is recycling an embryonic factor to induce brain plasticity," says Dr. Hensch.
Hensch not wants to study the transport mechanism that propagates Otx2 from the retina to the cortex.
He speculates that Otx2 itself could be a carrier for factors one would want to deliver to the brain, envisioning eye drops for brain disorders such as schizophrenia, in which parvalbumin cells do not properly mature.