Steven J. Tavalin

This study manipulates CaMKII activity in zebrafish retinal rod bipolar cell ribbon synapses to show that both inhibition and elevation impair neurotransmitter release, suggesting optimal CaMKII levels are required for normal function.

This study identifies GluN3A-NMDA receptors as negative regulators of GIT1/mTORC1 assembly, showing their role in controlling synaptic protein synthesis and memory formation.

The paper shows that NMDAR activation leads to input-specific potentiation of dendritic GABAergic inhibition via somatostatin interneurons, requiring CaMKII and GABA-A β2-subunit, and highlights its role in maintaining synaptic balance.