Actin remodeling, the synaptic tag and the maintenance of synaptic plasticity.

Activity-dependent plasticity of synaptic connections is a hallmark of the mammalian brain and represents a key mechanism for rewiring neural circuits during development, experience-dependent plasticity, and brain disorders. Cellular models of memory, such as long-term potentiation and long-term depression, share common principles to memory consolidation. As for memory, the maintenance of synaptic plasticity is dependent on the synthesis of de novo protein synthesis. The synaptic-tagging and capture hypothesis states that the maintenance of synaptic plasticity is dependent on the interplay between input-specific synaptic tags and the allocation or capture of plasticity-related proteins (PRPs) at activated synapses. The setting of the synaptic tag and the capture of PRPs are independent processes that can occur separated in time and different groups of activated synapses. How are these two processes orchestrated in time and space? Here, we discuss the synaptic-tagging and capture hypothesis in the light of neuronal compartmentalization models and address the role of actin as a putative synaptic tag. If different groups of synapses interact by synaptic-tagging and capture mechanisms, understanding the spatial rules of such interaction is key to define the relevant neuronal compartment. We also discuss how actin modulation can allow an input-specific capture of PRPs and try to conciliate the temporal dynamics of synaptic actin with the maintenance of plasticity. Understanding how multiple synapses interact in time and space is fundamental to predict how neurons integrate information and ultimately how memory is acquired.