Lynx for Braking Plasticity

+ See all authors and affiliations

Science  26 Nov 2010:
Vol. 330, Issue 6008, pp. 1189-1190
DOI: 10.1126/science.1198983

You are currently viewing the summary.

View Full Text


The juvenile brain exhibits a high capacity for plasticity and repair that is severely restricted in adulthood. In young mammals, for instance, classic experiments have shown that closing one eye for several days (monocular deprivation) leads visual cortex neurons to shift their responses toward sensory inputs originating from the other, nondeprived eye (1). In adults, however, such plasticity in ocular dominance, while not eliminated, is strongly restricted. This knowledge gap has medical implications, because the restoration of juvenile plasticity in injured or dysfunctional adults has the potential to allow recovery of neurological performance. On page 1238 of this issue, Morishita et al. (2) identify one brake on visual cortex plasticity in adults: Lynx1, a protein that inhibits nicotinic acetylcholine receptors (nAChRs). By eliminating the gene that expresses Lynx1 in mice, the researchers were able to create adult animals that exhibited visual cortex plasticity similar to that exhibited by juveniles.