Elucidation of molecular mechanism of synaptic plasticity by kinetic analysis of receptor trafficking

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Long-term depression (LTD) of synaptic transmission provides a mechanism of motor leaning, and as a mechanism of LTD, destabilization and consequent elimination of glutamate receptor (GluR) via endocytosis has been proposed, however, no quantitative examination has been performed. Here, stable pool size of GluR and its destabilization upon LTD was quantified, and rate constant of endocytosis of GluR was measured and compared between before and after LTD-induction. Then, I developed a mathematical model of GluR trafficking upon LTD, which predicts partial loss of recycling internal pool of GluR. Image analysis of GluR, tagged by fluorescent protein, indicated translocation of internal GluR from the spine to the dendritic shaft upon LTD, which is consistent with the prediction by the mathematical model of GluR trafficking in cerebellar Purkinje cell.