Abstract
Recent data indicate that plasticity protocols have not only synapse-specific but also more widespread effects. In particular, in synaptic tagging and capture (STC), tagged synapses can capture plasticity-related proteins, synthesized in response to strong stimulation of other synapses. This leads to long-lasting modification of only weakly stimulated synapses. Here we present a biophysical model of synaptic plasticity in the hippocampus that incorporates several key results from experiments on STC. The model specifies a set of physical states in which a synapse can exist, together with transition rates that are affected by high- and low-frequency stimulation protocols. In contrast to most standard plasticity models, the model exhibits both early- and late-phase LTP/D, de-potentiation, and STC. As such, it provides a useful starting point for further theoretical work on the role of STC in learning and memory.
Highlights
It is widely believed that synaptic potentiation, as demonstrated by the physiological phenomenon of long-term potentiation (LTP), plays an important role in memory formation in the brain [1,2]
Our convention is to say that states are distinct if they differ either in their synaptic strength or in the expected time it will take them to potentiate or depress in the absence of any plasticity protocols. This leads us to a six state model, containing three weak and three strong states: weak basal, strong basal, e-long-term depression (LTD), e-LTP, ‘-LTD and ‘-LTP
To model synaptic tagging and capture (STC), certain stimulation protocols given to just one population of synapses can affect the transition rates of multiple populations
Summary
It is widely believed that synaptic potentiation, as demonstrated by the physiological phenomenon of long-term potentiation (LTP), plays an important role in memory formation in the brain [1,2] This has triggered a vast number of experiments in which this phenomenon has been recorded, both in vivo and in vitro. There is an ‘‘early’’, transient phase (e-LTP) that can be induced by a single, brief (*1s), burst of high-frequency stimulation (weak HFS). The lifetime of this phase is around three hours in slice experiments, and its expression does not require protein synthesis [4,5,6]. It has been shown that protein synthesis is triggered at the time of induction and is necessary for ‘-LTP [4,5], a more complicated role for protein synthesis in LTP has been implied [10,11]
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