Expression of constitutively active CaMKII in target tissue modifies presynaptic axon arbor growth.

Calcium/calmodulin-dependent protein kinase II (CaMKII) can be regulated by synaptic activity and could therefore be involved in activity-dependent control of neuronal growth. We tested whether increased CaMKII activity in postsynaptic optic tectal neurons can modify the development of retinotectal axons in Xenopus. The elaboration of individual presynaptic retinal axons was observed in vivo before and up to 3 days after infecting the tectal cells with vaccinia virus carrying the gene for constitutively active truncated CaMKII (tCaMKII). Elevated postsynaptic CaMKII activity prevented the axons from developing the complexity of normal arbors by increasing the normal rate of branch retractions. Some effects of tCaMKII on arbor morphology were seen 1 day after infection, but they became more dramatic by the third day. The results suggest that postsynaptic CaMKII plays a role in the development of presynaptic arbor structure.