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Solving the puzzle of the BK ion channel

tage, or potential difference, across the membrane. Ligand-gated channels are triggered by the binding of a chemical messenger, such as calcium. The BK channel's gate responds to both types of stimuli.

Normally action potentials aren't strong enough to trip the BK channel's gate. But each action potential lets calcium ions into the cell. At higher calcium concentrations, the BK channel's voltage threshold is shifted to lower voltages. Now action potentials can trip the gate, opening the BK channel.

The BK channel, also called the Big K channel or MaxiK channel, lets about 200,000 potassium ions through a millisecond, roughly 20 times more than a typical potassium channel. So when the BK channels open, they quickly repolarize the membrane, lopping off the action potential.

How might a BK channel mutation lead to epilepsy? Because the mutation allows the membrane to repolarize more quickly, the nerve cell can fire at higher frequencies, an excitability that may lead to seizures.

Cui emphasizes, however, that the link between the mutation and epilepsy has not been fully worked out.

The channel's structure and mechanics

The various parts of the channel are only loosely associated, like chunks of pull-apart bread, and the voltage and calcium sensors are at some distance from the pore. So it is not at first clear how changes in the electrical field or the binding of calcium ions open the pore.

The voltage sensor includes a helix that is loaded with several copies of the positively charged amino acid arginine. The electric field across the membrane works on these positive charges, pushing the helix out of the membrane or pulling it deeper in, depending on the field's polarity.

When it is pushed up, the helix pulls on the linker chain that connects the bottom of the voltage sensor to the bottom end of a helix in the pore. So pushing the charged helix up opens the pore, and pushing it down closes th

Contact: Diana Lutz
Washington University in St. Louis

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