A molecular brake controls the magnitude of long-term potentiation

Yubin Wang, Guoqi Zhu, Victor Briz, Yu-Tien Hsu, Xiaoning Bi and Michel Baudry ()
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Yubin Wang: Graduate College of Biomedical Sciences, Western University of Health Sciences
Guoqi Zhu: Graduate College of Biomedical Sciences, Western University of Health Sciences
Victor Briz: Graduate College of Biomedical Sciences, Western University of Health Sciences
Yu-Tien Hsu: Stanford Institute of NeuroInnovation and Translational Neuroscience, Stanford University
Xiaoning Bi: College of Osteopathic Medicine of the Pacific, Western University of Health Sciences
Michel Baudry: Graduate College of Biomedical Sciences, Western University of Health Sciences

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract Overexpression of suprachiasmatic nucleus circadian oscillatory protein (SCOP), a negative ERK regulator, blocks long-term memory encoding. Inhibition of calpain-mediated SCOP degradation also prevents the formation of long-term memory, suggesting rapid SCOP breakdown is necessary for memory encoding. However, whether SCOP levels also control the magnitude of long-term synaptic plasticity is unknown. Here we show that following synaptic activity-induced SCOP degradation, SCOP is rapidly replaced via mTOR-mediated protein synthesis. We further show that early SCOP degradation is specifically catalysed by μ-calpain, whereas late SCOP resynthesis is mediated by m-calpain. We propose that μ-calpain promotes long-term potentiation induction by degrading SCOP and activating ERK, whereas m-calpain activation limits the magnitude of potentiation by terminating the ERK response via enhanced SCOP synthesis. This unique braking mechanism could account for the advantages of spaced versus massed training in the formation of long-term memory.

Date: 2014
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DOI: 10.1038/ncomms4051

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