Fig. 9

Contribution of reactive OPCs to zebrafish spinal cord regeneration. (A) In the unlesioned spinal cord, oligodendrocytes ensheath axons and OPCs have thin bipolar processes. Non-myelinated axons and other cell types are omitted for figure clarity. (B) Oligodendrocytes are lost acutely upon lesion, but cellular debris is removed by activated immune cells. OPCs become reactive, proliferate and systemically upregulate genes related to differentiation. A proportion of reactive OPCs becomes pre-myelinating, directly supporting spared axons. (C) Both oligodendrocyte progenitor and oligodendrocyte cell numbers are re-established. At 42 dpl, (re-)myelination is not fully completed, with myelin sheaths that are as yet thinner, compared to pre-injury levels. Some axons are degenerating, while others are still non-myelinated. Nevertheless, partial anatomical and molecular recovery is already sufficient to support the previously reported robust functional recovery at this point in time after lesion (Becker et al., 1997).