Analysis of axon divergence at the optic chiasm in nogo-a knockout mice.

Our earlier studies have shown that the axon growth inhibitory molecule Nogo affects axon routing at the optic chiasm likely through a differential regulation of Nogo receptor on the optic axons. Using isoform specific antibodies, we further showed that Nogo-A was predominantly expressed by retinal ganglion cells and their axons, while Nogo-B was highly localized on the radial glia at the midline of the chiasm, suggesting a role of Nogo-B in regulating turning of uncrossed axons. To further investigate the roles of Nogo-A in axon divergence, we analyzed the routing of axons in the chiasm of Nogo-A knockout mice during the growth of axons across the midline. At E13 to E16, there was no significant difference in the contralateral projection (P = 0.6943 for E13; P = 0.9867 for E14; P = 0.4121 for E15 and P = 0.3402 for E16). The results also showed the absence of Nogo-A did not cause any obvious change to the ipsilateral projection at the optic chiasm, both for the early generated uncrossed axons at E13 and E14 and the late cohorts at E15-E16, when compared with the wild-type mice (P = 0.4788 for E13; P = 0.188 for E14; P = 0.3152 for E15 and P = 0.432 for E16). These findings support that Nogo-A is not the major isoform to guide the axon divergence in the mouse optic chiasm.