Immature neurons of an embryonic or a perinatal brain reveal spontaneous Ca2+ activity even before they form synapses and are integrated into a functional circuit.Although such Ca2+ activity may play essential roles during multiple stages of neuronal circuit formation, the downstream Ca2+-dependent molecular mechanisms are still poorly understood.To address this question, we have systematically examined whether components of CaMKK-CaMKI (Ca2+/calmodulin-dependent protein kinase I) pathways contributed to these processes.