Journal
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
Volume 77, Issue -, Pages 43-50Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2017.09.025
Keywords
Long-term potentiation; Long-term depression; Synaptic tagging and capture; Inverse synaptic tagging; CaMKII; AMPA receptors
Categories
Funding
- Shionogi CO., LTD
- JSPS [15H04258, 15H02358, 16H01268, 17H06312]
- MEXT
- Takeda Science Foundation
- Nakatani Foundation
- Brain Science Foundation
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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. (C) 2017 Elsevier Ltd. All rights reserved.
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