2021 Volume 33 Issue 193 Pages E51-E54
Once a mammalian central nervous system axon is severed, it never regenerates. As a result, the neural circuit carried by this axon is permanently disrupted, and the dysfunction of that circuit remains a serious sequela for life. This is because chondroitin sulfate produced by glial scars caused by central nervous system injury functions as a potent axonal regeneration inhibitor. Although chondroitin sulfate induces an abnormal structure called dystrophic endball at the tip of axon via the neural cell receptor PTPRσ and inhibits its elongation, its detailed mechanism of operation has been unknown. In this review, we would like to outline the mechanism of axon regeneration inhibition by chondroitin sulfate, which was recently clarified by the authors.