The Ion Channel

Recent Finding Puts a Charge in Nerve Cell Studies

In the 1950s, two scientists at Cambridge University, Alan Hodgkin and Andrew Huxley, described how certain proteins acted as gateways for "channeling" potassium ions across the membranes of cells. The discovery was a stunning breakthrough, one that helped illuminate the mechanism by which electrical impulses from the spinal cord power up the body's cells. Subsequent research confirmed the importance of these "ion channels." Hodgkin and Huxley went on to win the Nobel Prize.

Scientists around the world, meanwhile, have built on their legacy to learn more about how ion channels make possible some of the fundamental processes of life itself, including sensory transduction, action-potential generation and muscle contraction.

One of the more surprising contributions has come from David Schulz, an assistant professor of biological sciences at MU. In a paper published last summer in the Proceedings of the National Academy of Sciences, Schulz and his co-authors described how variations in the number and arrangement of ion channels can allow different nerve cells to perform similar tasks -- a discovery that flew in the face of what the researchers call the "standard blueprint" for nerve cell functionality.

"The work that we're doing shows that you can get exactly the same output in these nerve cells, but the cells can be built differently," says Schulz. "They can use different ion channels or different amounts of ion channels as long as these cells are doing the right thing, which is key for what the brain and the spinal cord need to accomplish."

The finding, by shedding light on how normal nerve cells process ions, could one day help researchers coax healthy neurons into "compensating" for disrupted ion activity in cells damaged by injury or disease. "For example," Schulz says, "we're starting to uncover some of the compensatory mechanisms of what happens when you remove input to cells, what these ion channels might do, and how they might be co-regulated and altered in order to increase or decrease the cell's excitability. With these compensatory mechanisms could be implications for understanding spinal-cord injury or even epilepsy."

Published by the Office of Research.

©2008 Curators of the University of Missouri. Click here to contact the editor.