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ePoster
TAU CONTROLS THE HOMEOSTASIS OF SYNAPTIC NMDA RECEPTORS IN NEURONS
Xuan Ling Hilary Yongand 10 co-authors
The University of Queensland
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-008
Presentation
Date TBA
Board: PS01-07AM-008
Event Information
Poster Board
PS01-07AM-008
Poster
View posterAbstract
Dysregulation of the microtubule-associated protein tau causes synaptic deficits associated with a range of neurodegenerative diseases. However, the physiological function of tau at the postsynaptic compartment of neurons remains unclear. Here, we show that tau phosphorylation, distinct from its pathological form, is tightly regulated to control the subunit-specific expression of N-methyl-D-aspartate (NMDA) receptors during homeostatic plasticity. Upon chronic neuronal inactivity, tau is phosphorylated at Ser-235 by cyclin-dependent kinase 5, which helps retain active fyn kinase at the synapse. This promotes the phosphorylation of the GluN2B subunit of NMDA receptors at Tyr-1472, thereby increasing receptor availability at synapses during homeostatic adaptation. Moreover, disease-associated tau mutations cause an aberrant increase in surface NMDA receptor levels, which can be restored by blocking tau phosphorylation at Ser-235. Together, our findings identify a physiological role for tau in homeostatic synaptic plasticity, the perturbation of which can lead to neuronal hyperexcitation, seizures and excitotoxic cell death.
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