Abstract
Synaptic plasticity, a fundamental memory mechanism, involves changes in glutamate receptor expression. Our lab previously demonstrated the memory-enhancing neuromodulator, soluble amyloid precursor protein-alpha (sAPPα), regulates cell surface expression of GluN1, the obligatory subunit of NMDA-glutamate receptors.
Here, we aimed to explore sAPPα’s effect on GluN1 surface expression and synaptic localisation across time, hypothesising that sAPPα would initially enhance and later repress GluN1 expression, reflecting sAPPα’s neuromodulatory properties.