Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8479672 | Seminars in Cell & Developmental Biology | 2018 | 8 Pages |
Abstract
Long-lasting forms of synaptic plasticity such as long-term potentiation (LTP) and long-term depression (LTD) are fundamental cellular mechanisms underlying learning and memory. The synaptic tagging and capture (STC) hypothesis has provided a theoretical framework on how products of activity-dependent genes may interact with potentiated synapses to facilitate and maintain such long-lasting synaptic plasticity. Although Arc/arg3.1 was initially assumed to participate in STC processes during LTP, accumulating evidence indicated that Arc/arg3.1 might rather contribute in weakening of synaptic weights than in their strengthening. In particular, analyses of Arc/Arg3.1 protein dynamics and function in the dendrites after plasticity-inducing stimuli have revealed a new type of inactivity-dependent redistribution of synaptic weights, termed “inverse synaptic tagging”. The original synaptic tagging and inverse synaptic tagging likely co-exist and are mutually non-exclusive mechanisms, which together may help orchestrate the redistribution of synaptic weights and promote the enhancement and maintenance of their contrast between potentiated and non-potentiated synapses during the late phase of long-term synaptic plasticity. In this review, we describe the inverse synaptic tagging mechanism that controls synaptic dynamics of Arc/Arg3.1, an immediate early gene product which is captured and preferentially targeted to non-potentiated synapses, and discuss its impact on neuronal circuit refinement and cognitive function.
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Authors
Hiroyuki Okuno, Keiichiro Minatohara, Haruhiko Bito,