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A protein called RNF10 relays messages from synapses to neuron cell nuclei, and is responsible for long-lasting modifications of dendritic spines as observed after activation of synaptic glutamate receptors.

NMDA receptor function is regulated by protein depalmitoylation during visual cortical maturation and is dysfunctional in infantile neuronal ceroid lipofuscinosis.

The APP intracellular domain (AICD) physiologically regulates synaptic GluN2B-containing NMDA receptor current, a process that could contribute to pathological Alzheimer's disease-related synaptic failure upon increase of AICD levels in adult neurons.

An activity-dependent mechanism sculpts subcellular segregation of sensory inputs.

Individual neurons can adjust the strength of their synapses by using spontaneous calcium influx through NMDA receptors to trigger the release of additional calcium from intracellular stores, which can in turn be used to regulate protein synthesis.

Novel spatial representations by hippocampal cellular assemblies develop on the framework of preconfigured hippocampal networks whose homeostatic synaptic reorganization is accelerated by prior experience and CA3 NMDAR-dependent plasticity.

Electrophysiology experiments with genetic and pharmacological manipulations identify a role for astrocyte GluN2C NMDA receptors in maintaining the broad range of presynaptic strengths, which is suggested by numerical simulations to enhance the expression of synaptic plasticity.

Non-conventional NMDA receptors containing GluN3A subunits place constraints on the capacity of the brain to encode lasting memories through regulation of synaptic GIT1/mTOR signaling complexes.

In a population of mammalian central synapses, spontaneous and evoked neurotransmitter release processes are independently distributed; yet, postsynaptic receptors within a single synapse preferentially receive neurotransmitter from only one mode of release.

Prediction error responses in layer 2/3 of mouse visual cortex are shaped by experience-dependent modifications of the local cortical circuit.