These molecules dock at specific places, or receptors, on the cell and trigger "channels" in the cell's membrane to open. Depending on the receptor and the channel, in will flow sodium, calcium, chloride or other charged atoms that then keep the communication process going.
In the cells in the cerebellum, a channel made of proteins called AMPA receptors, built from subunits called GluR3 and GluR4, is usually found at the synapse. If the cells are shocked with an electric current, within minutes the channels are replaced by ones made of GluR2 and GluR3. After the swap, sodium can still get in, but calcium is kept out.
To learn more about how this takes place, the Hopkins researchers studied brain cells from genetically engineered mice. Through their experiments, the researchers determined that the PICK1 and NSF proteins are both required for the calcium-forbidding channel to move into place at the synapse. Exactly how they help the channels move is still unknown, as is why the cells change their channels.
Part of the answer is likely to be self-preservation: Too much calcium inside nerve cells can kill them. But Huganir points out that calcium does a lot of things inside cells, suggesting that the channel swap might be accomplishing more than just keeping the cell alive. "Calcium turns some processes on, and it turns others off," he says. "My personal belief is that the cells might be doing more than just protecting themselves by keeping calcium out."
In some cases, protection might be enough of a goal. In people with Lou Gehrig's disease, or amyotrophic lateral sclerosis (ALS), some muscle-controlling nerve cells die because too much of the brain chemical glutamate binds to the cells' AMPA receptors,