MMP2 and MMP9 Activity Is Crucial for Adult Visual Cortex Plasticity in Healthy and Stroke-Affected Mice

A fundamental regulator of neuronal network development and plasticity is the extracellular matrix (ECM) of the brain. The ECM provides a scaffold stabilizing synaptic circuits, while the proteolytic cleavage of its components and cell surface proteins are thought to have permissive roles in the regulation of plasticity. The enzymatic proteolysis is thought to be crucial for homeostasis between stability and reorganizational plasticity and facilitated largely by a family of proteinases named matrix metalloproteinases (MMPs). Here, we investigated whether MMP2 and MMP9 play a role in mediating adult primary visual cortex (V1) plasticity as well as stroke-induced impairments of visual cortex plasticity in mice. In healthy adult mice, selective inhibition of MMP2/9 for 7 d suppressed ocular dominance plasticity. In contrast, brief inhibition of MMP2/9 after a cortical stroke rescued compromised plasticity. Our data indicate that the proteolytic activity of MMP2 and MMP9 is critical and required to be within a narrow range to allow adult visual plasticity.

Automated summary

The extracellular matrix (ECM) plays a crucial role in neuronal network development and plasticity. Proteolytic cleavage of ECM and cell surface proteins is important for regulating plasticity. MMP2 and MMP9 are enzymes involved in proteolysis and their activity is critical for adult visual plasticity.