John A. Gray

D-Serine inhibits non-ionotropic NMDA receptor signaling

This study shows that D-serine inhibits non-ionotropic NMDA receptor signaling and plasticity by blocking glutamate-induced conformational changes in the absence of co-agonist.

Reduced D-serine levels drive enhanced non-ionotropic NMDA receptor signaling and destabilization of dendritic spines in a mouse model for studying schizophrenia

The paper shows that reduced D-serine in a schizophrenia mouse model enhances non-ionotropic NMDAR signaling, leading to dendritic spine destabilization.

Increased excitation-inhibition balance due to a loss of GABAergic synapses in the serine racemase knockout model of NMDA receptor hypofunction

The paper investigates the relationship between NMDA receptor hypofunction and GABAergic synapse loss in SRKO mice, finding reduced inhibitory synapses and increased excitation-inhibition imbalance.

Postsynaptic serine racemase regulates NMDA receptor function

This study shows that postsynaptic serine racemase regulates NMDA receptor function in mouse hippocampal neurons, with age-dependent effects on long-term potentiation and GluN2B expression.

NMDAR-activated PP1 dephosphorylates GluN2B to modulate NMDAR synaptic content.

The paper identifies phosphorylation of GluN2B at S1480 as a mechanism controlling NMDAR synaptic content through PP1-mediated dephosphorylation.

Long-term depression is independent of GluN2 subunit composition.

This study shows that neither GluN2A nor GluN2B subunits are strictly required for non-ionotropic or ionotropic long-term depression.