It turns out that the mutation makes part of the channel more rigid, altering its dynamics in a way that makes it easier to toggle it open. This is the first time, says Cui, that protein dynamics have been implicated in the functioning of an ion channel.
Life itself depends on ion channels, the tiny pores in our cells that open on cue, letting charged atoms rush in or out. These influxes and effluxes create the electrical signals that make our eyes blink or our ribs expand to draw breath.
But because the channels are tiny and stuck in the greasy cell membrane, they are hard to study. Their existence wasn't even confirmed until the 1970s. Working out the structure and function of a single ion channel (there are more than 300 types) earned researchers a Nobel Prize as recently as 2003.
Nerve impulses are actually changes in the electrical potential across a nerve cell's membrane. The traveling wave of electrical excitation, known as an action potential, is orchestrated by the synchronized opening and closing of ion channels.
At rest, cells are slightly more negative (a matter of millivolts) inside than they are outside. An action potential starts when sodium channels open, allowing positively charged sodium atoms to rush into the cell, reversing the polarization of the membrane.
The sodium channels then automatically close and potassium channels open, repolarizing the membrane by allowing positively charged potassium ions to flood out of the cell.
What the BK channel does
One of the BK channel's functions is to allow a nerve to adapt to constant stimulation by becoming less responsive. This loss of sensitivity is what allows us, for example, to ignore the constant pressure of our clothing.
Ion channels are gated, or triggered, in a variety of ways. Voltage-gated channels respond to the vol
|Contact: Diana Lutz|
Washington University in St. Louis