of inhibitory neurons in the central nervous system, appearing with age to stabilize mature circuits. PNN development coincides with the closure of critical periods, and both PNN formation and critical period timing is delayed in dark-rearing. For example, PNN digestion by ABC chondroitinase in rats leads to a shift in ocular dominance upon monocular deprivation, which is normally restricted to its critical period much earlier in development. Additionally, PNNs are negatively charged, which is theorized to create a cation-rich environment around cells, potentially leading to an increased firing rate of inhibitory neurons, thereby allowing for increased inhibition after the formation of PNNs and helping to close the critical period. The role of PNNs in critical period closure is further supported by the finding that fast-spiking parvalbulmin-positive interneurons are often surrounded by PNNs. Perineuronal nets have also been found to contain chemorepulsive factors, such as semaphorin3A, which restrict axon growth necessary for plasticity during critical periods. In all, these data suggest a role for PNNs in the maturation of CNS inhibition, the prevention of plastic axonal growth, and subsequently, critical period closure. Myelin Another mechanism that closes the critical period is myelination. Myelin sheaths are formed by oligodendrocytes in the CNS that wrap around segments of axons to increase their firing speed. Myelin is formed in the early stages of development and progresses in waves, with brain areas of later phylogenetic development (i.e. those associated with “higher” brain functions like the frontal lobes) having later myelination. The maturation of myelination in intracortical layers coincides with critical period closure in mice, which has led to further research on the role of myelination on critical period duration. Myelin is known to bind many different axonal growth inhibitors that prevent plasticity seen in critical periods. The Nogo Receptor is expressed in myelin and binds to the axonal growth inhibitors Nogo and MAG (among others), preventing axon growth in mature, myelinated neurons. Instead of affecting the timing of the critical period, mutations of the Nogo receptor prolong the critical period temporarily. A mutation of the Nogo receptor in mice was found to extend the critical period for monocular dominance from around 20 – 32 days to 45 or 120 days, suggesting a likely role of the myelin Nogo receptor in critical period closure. Additionally, the effects of myelination are temporally limited, since myelination itself may have its own critical period and timing. Research has shown