The interplay between neuronal activity and actin dynamics in synaptic tagging and capture
Long-lasting forms of plasticity, such as long-term potentiation (LTP) or long-term depression (LTD) require the allocation of plasticity-related proteins (PRPs) in an input-specific manner - synaptic tagging and capture. I will present recent evidence from our laboratory supporting the hypothesis that the synaptic tag is a transient state of the synapses that allows plasticity to occur. I will also show that the modulation of synaptic actin cytoskeleton is necessary for the induction of LTP and LTD and it is involved in synaptic tagging and capture in LTD and LTP. Interestingly, pharmacological modulation of the actin cytoskeleton can create an artificial synaptic tag that can capture PRPs. The dynamics of the actin cytoskeleton is activity-dependent and modulated by CaMKII activation. These observations strengthen our hypothesis that modulation of actin is a general mechanism that provides an input-specific signal for PRPs capture and is independent of the upstream events triggered by LTP or LTD induction. We are now imaging actin dynamics, using STED microscopy, to analyse our homo-synaptic and hetero-synaptic forms of plasticity modulate the synaptic actin cytoskeleton.
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