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Translational switch for long term maintenance of synaptic plasticity
© Aslam et al; licensee BioMed Central Ltd. 2008
Published: 11 July 2008
Memory lasts a lifetime, yet the physiological substrate of memory, synaptic contacts, are composed of proteins that have much shorter lifetimes. A physiological analog of memory formation, long-term potentiation (LTP), has a late protein synthesis dependent phase (L-LTP) that can last for many hours in slices, or even days in vivo. Could the activity dependent synthesis of new proteins account for persistence of L-LTP and memory? Here, we examine the proposal that a self-sustaining regulation of translation can form a bistable switch that can persistently regulate the on-site synthesis of plasticity related proteins. We show that a αCaMKII-CPEB1 molecular pair can operate as a bistable switch. Our results imply that L-LTP should produce an increase in the total amount of αCaMKII at potentiated synapses. This paper also proposes an explanation for why the application of protein synthesis and αCaMKII inhibitors at the induction and maintenance phases of L-LTP result in very different outcomes.
This model, of a translational switch relies on the self sustained regulation of translation and can support both synaptic specificity and stability.
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