Long-term potentiation (LTP) relies on coordinated kinase activity, including CaMKII and ERK, to regulate synaptic strength through AMPA receptor function and trafficking. This study investigated calcium-dependent ERK activation, identifying the CaMKK/CaMKI pathway as a potential link between NMDA receptor signaling and ERK during LTP. Additionally, the role of small G-proteins, particularly Rac1 and its effector WAVE-1, was examined in synaptic plasticity and actin remodeling. Findings suggest that WAVE-1 influences dendritic structure and a novel form of synaptic regulation termed capacitative metaplasticity, offering new insight into mechanisms underlying learning and memory.
