Silent synapse

Normal transmission across a glutamatergic synapse relies on the neurotransmitter glutamate, the glutamate-specific AMPA receptor (AMPAR), and calcium ions.

This magnesium binding site is located in the pore of the channel, at a place within the electrical field generated by the membrane potential.

This gives the NMDAR the property of being voltage-dependent, in that it requires strong postsynaptic depolarization to allow ion flux.

Silent synapses were proposed as an explanation for differences in quantal content of excitatory postsynaptic currents (EPSCs) mediated by AMPARs and NMDARs in hippocampal neurons.

Moreover, the EPSCs elicited with depolarized membrane potentials can be completely blocked by D-APV, a selective NMDAR blocker.

[4] Silent synapses are activated via the insertion of AMPARs into the postsynaptic membrane, a phenomenon commonly called "AMPA receptor trafficking.

Calmodulin activates calcium/calmodulin-dependent protein kinase II (CaMKII), which — among other things — acts on AMPAR-containing vesicles near the postsynaptic membrane.

The Role of Silent Synapses in Long Term Potentiation Neural Development AMPA Receptor Trafficking