Neurons communicate with each other at synapses, and it’s largely a chemical signal, though electrical signals (gap junctions) do exist and are important in their own rite. Now one model of learning and memory involves the dynamic change of these synapses due to activity. These so-called activity-dependent changes — plasticity — require that something physically changes at the synapse. That is to say, somehow, the neurons are communicating more or more effectively.
One way neurons do this post-synaptically is becoming clear. AMPA receptors, the major non-NMDA type of glutamate receptor, have been observed and subsequently modeled to be actively trafficked into and out of the membrane at a synapse. Since these AMPA receptors are also implicated in forms of plasticity such as long term potentiation (LTP), this AMPA receptor trafficking provides at least one piece of the mechanism by which activity dependent changes might occur.
While the details of the AMPA receptor trafficking mechanism become more and more clear, it is interesting to ask whether or not there might be a more generalizable mechanism by which the surface expression of ANY receptors might be similarly regulated. It would make a lot of sense if the method was the same with different details. This idea is kind of extrapolated from the abstract of this article.