Figure 7.

Wnt/calcium signaling guiding axon growth through the corpus callosum. (A) A schematic of a cortical slice showing cortical axons extending through the corpus callosum (CC) around which Wnt5a is expressed in the induseum griesium (IG) and glial wedge (GW). Axons in the contralateral callosum have high frequencies of calcium transients caused by Wnt5a signaling which accelerate rates of axon outgrowth. In contrast, ipsilateral axons, which are not yet responsive to Wnt5a, have little calcium activity and therefore grow more slowly. LV, lateral ventricle; CP, cortical plate. (B) A schematic of intracellular signaling in the post-crossing axon from (A). A Wnt5a gradient from the glial wedge activates Ryk receptors to open IP3 receptors and TRP channels, causing release of calcium from intracellular stores and calcium influx through the plasma membrane. These transients activate CaMKII to accelerate axon extension and repel growth cones away from the glial wedge toward the contralateral cortical plate.