Dendritic spine dynamics stabilize synaptic plasticity

Long-term synaptic plasticity is believed to underlie learning and memory in the brain. At excitatory synapses, plasticity is mediated by molecular machinery that detects local calcium (Ca2+) signals in small structures called dendritic spines. For unknown reasons, spine size is tightly correlated with synaptic strength. We show theoretically that imperfect coupling between spine size and Ca2+ influx fundamentally alters synaptic stability. If Ca2+ influx is under-compensated, then strong synapses are stabilized and synaptic strength distributions are unimodal. In contrast, over-compensation of Ca2+ influx leads to binary, persistent synaptic strengths with bimodal distributions. We conclude that structural plasticity provides a simple, local and general mechanism that allows dendritic spines to foster both rapid memory formation and persistent memory storage.