At the heart of how we are able to think lies a problem in the organization of molecules on cell membranes. It is now generally accepted that the ability of our nervous systems to learn and change reflects an underlying ability of cells of the nervous system to dynamically alter the strengths of their connections. These connections, called synapses, are cell surface specializations containing functional and structural molecules at very high local concentrations. One very important way by which synaptic strength can be modulated is by changing the size of the synapses. In general, bigger synapses are stronger synapses.
Synapses become bigger by recruiting more constituent molecules.
Although, many of these molecules have now been identified at the model synapse of choice, the neuromuscular junction, how they aggregate and disperse at a synaptic connection remains a complete mystery. My colleagues and I are taking a two-pronged approach to the problem. First, we are using a muscle cell culture model in which we can observe the aggregation of known synaptic molecules in response to neurons or active factors such as neural agrin. When observed in detail, the aggregation is quite dynamic in surprising ways that we hope will promote a better understanding of the underlying processes. In a second approach, we have taken to modeling what we know about the molecular players and exploring whether these properties in conjunction with a minimum of assumptions can indeed produce aggregates that behave similarly to those seen in living cells.