Research ArticleNeuroscience

Blocking PirB up-regulates spines and functional synapses to unlock visual cortical plasticity and facilitate recovery from amblyopia

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Science Translational Medicine  15 Oct 2014:
Vol. 6, Issue 258, pp. 258ra140
DOI: 10.1126/scitranslmed.3010157

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In Search of a Young and Supple Brain

It is easy to learn a language as a small child, but not so easy as an adult. Similarly, children who are born with certain defects in one eye can recover vision in that eye if it’s corrected early in childhood, but not if it’s corrected too late. Bochner et al. now report a way to unlock youthful brain plasticity in adult mice. Blocking a cell surface receptor called PirB (initially characterized as an innate immune receptor) found on neurons in the cortex, either genetically or biochemically, allowed the animals to rapidly adjust to the loss of sight in one eye—just as if it were a young pup. A closer look revealed new, functional synapses and extra synapse-containing spines on the neurons. Even mice that were blind in one eye for a long time, mimicking human amblyopia, could adapt and compensate after inhibition of PirB. This ability to enhance neural plasticity could be harnessed for recovery after brain injury or for correction of developmental disorders.

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