Hensch and his collaborators have now found that basket-cell development is controlled by a protein called Otx2. Overexpressing this protein can trigger a critical period of plasticity, while removing Otx2 halts it. While the findings are specific to the visual system, Hensch notes that different sensory systems also possess basket cells, and those might function the same way.

A second mechanism for manipulating neural plasticity in adults is blocking inhibitory molecules that the nervous system produces to stop neural growth. “The nervous system is hostile to growing new axons [the long neural projections that connect cells], which is why recovery after spinal-cord injury is so challenging,” says Hensch. 

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.)

     The article goes on, in brief, to explore the possible links between brain plasticity and autisim and the possible downsides of re-engaging the brain’s “plastic” state at later ages.    

You know, it’s not hard science by any stretch of the imagination, but I can’t help but think of Grant Morrison’s claims that A) Mr. Fantastic uses his powers to enhance his brain’s plasticity, and B) that Mr. Fantastic has Asperger Syndrome.