MBL summer investigator Clay Armstrong, a professor of physiology at the University of Pennsylvania's School of Medicine, is looking at the role of calcium in the transmission of electrical impulses in squid nerves. His work aims to expand our knowledge of how nerves operate in both squids and humans. Work performed on squid giant axons in the late 1930s and '40s forms the basis for virtually everything that is known about the electrical activity of the brain and the heart.

Scientists now know that when an electrical impulse passes through the nervous system, it sweeps along the surface membranes of nerve fibers. These membranes contain large numbers of "gated" channels. When the gates open, ions flow rapidly in or out of the cell.

Only certain ions are allowed to pass through the gates, however. This selectivity divides the channels into two major groups: one that is specific for potassium ions. When the gates of sodium channels open, sodium ions, concentrated outside the membrane, rush into the nerve fiber and force a positive change of voltage internally. Open potassium channels force the membrane potential in the opposite direction, back to its negative resting level.

Each sodium channel is a protein molecule with a highly specialized structure that makes it exquisitely sensitive to membrane potential. With an influx of sodium ions, the positive voltage change causes a wave-like opening of sodium channels further along the fiber. This wave is the nerve impulse. The impulse lasts only a fraction of a millisecond; then the sodium gates close. To return the cell to its negative state, potassium channels gates open, allowing a rush of potassium ions to the outside of the cell.

After the impulse has passed, these is some mopping up to be done. The cell has gained some sodium ions and lost some potassium ions. The clean-up is performed by another specialized protein molecule, the sodium-potassium pump. The pump uses ATP, the cell's equivalent of gasoline, to push sodium ions out and bring potassium ions in.

Armstrong's hypothesis is that a closed channel contains a calcium ion that acts as a physical plug to ion movement. Opening of a channel involves the release of the calcium ion trapped in the channel, in addition to the twisting of the channel protein by movement of regions of high positive charge density. Conversely, the channel cannot close until it has bound a calcium ion.

This past summer, Armstrong's research focused on the role of calcium ions in gating sodium channels. The working hypothesis was that the gates of sodium channels would not close in the absence of calcium ions. Armstrong says that initial experiments look promising, but the effects of calcium ion are complex and difficult to sort out. In addition to binding in the channel, there may be other sites on the protein that interact with calcium.

Not everyone agrees with Armstrong's interpretation. Working one floor below his MBL lab last summer was long-time collaborator Francisco Bezanilla (known to all as Pancho), a Chilean physiologist now at UCLA. Benzanilla says his measurements indicate that sodium channels can close quite well at very low concentrations of calcium ion. The two scientists do not use the same technique to measure channel activity, however.

Armstrong expects that he and Bezanilla will eventually come to an agreement on calcium's role. "Pancho has some measurements indicating my theory is wrong. I have indicating I'm right. Furthermore, my theory ties together a lot of phenomena I've been worrying about for years. Ultimately, of course, we will work it out."

Whatever the details of calcium's role in the conduction of nerve impulses, it is not likely that people can tune up their calcium intake. Although a regular supply of calcium is essential, the body has a system for adjusting the calcium level in the blood that inures the body to fluctuations in daily dietary intake. In the case of acute emergencies, bones provide the body with a large reservoir of calcium.