| Summary: | It has been widely accepted that long-term potentiation (LTP) in the hippocampal CA1
region mostly results from increased insertion of post-synaptic α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs). The previous
study in our lab has shown that activation of phosphatidylinositol 3-kinase (PI3K) by
selective stimulation of synaptic N-methyl-D-aspartate receptors (NMDARs) is required
for the increased cell surface expression of AMPARs and the consequent LTP. However,
the following signaling pathways still remain unknown. In the present study, the
involvement of Akt, the primary downstream protein kinase of PI3K, was examined with
a combination of electrophysiological, biochemical and molecular biological techniques.
The study found that Akt is required for the post-synaptic AMPAR insertion and LTP.
Furthermore, the threonine 840 (Thr840) on GluRl C-tail was identified as a novel Akt
phosphorylation site, suggesting a potential mechanism by which Akt contributes to
AMPAR incorporation and LTP. === Medicine, Faculty of === Graduate
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