Molecular and cellular mechanisms of ocular dominance plasticity in adult induced by serine proteases

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To understand the molecular and cellular mechanisms of ocular dominance (OD) plasticity in adulthood, we explored candidate substrates of serine proteases, which are essential for morphological plasticity. Using mice during and after the CP for OD plasticity, we found proteolysis of extracellular matrix proteins and adhesion molecules including telencephalin (TLCN) by plasmin. Interestingly, telencephalin slowed spine maturation while plasmin enhanced synaptic formation, suggesting that there is a negative correlation between the full-length TLCN and plasmin.