John F. Wesseling

The paper shows that synaptophysin and synaptogyrin family proteins co-express with synapsin to generate small vesicles and that their absence leads to larger synaptic vesicles.

The paper shows that NMDA receptor-dependent LTP components can be occluded by altering baseline synaptic strength through Ca2+ manipulation in Synaptophysin family knockouts.

The paper confirms the existence of multiple reserve pools at hippocampal synapses with parallel organization, showing no intermixing even under intense stimulation.

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