New method to dampen nerve signals

What do the toxins from arrow-poison frogs, puffer fish and scorpions have in common with drugs against epilepsy? The answer is that they all affect the ability of nerves to transmit electrical impulses by affecting the ion channels in nerves. Ion channels are small openings in the cell membrane of nerves that open and close like doors, in order to allow electrically charged ions to enter or exit. When enough ions have flowed into the nerve cell, an electrical impulse is released and transmitted along the nerve. Sometimes, however, it becomes far too easy for an electrical impulse to be released. Increased electrical excitability of nerves lies behind such conditions as epileptic seizures, disturbances in heart rhythm, and the experience of pain.

The anti-epileptic medication currently in use, and the animal toxins mentioned above, reduce electrical excitability by closing a certain type of ion channel. All such previously known molecules bind to locations at the ion channel itself. These binding sites are generally surrounded by water. In contrast, the cell membrane that the ion channel passes through is built from a bilayer of lipids, which are a form of fat that repels water-soluble substances.

“We show that a small molecule is embedded into the lipid bilayer and has direct contact with the ion channel. This is a fundamentally different type of binding site. One interesting question is whether we have naturally occurring molecules in the body that bind to ion channels in the same way. We probably do,” says Fredrik Elinder, professor in the Department of Clinical and Experimental Medicine at Linköping University.

The findings are published in the journal Science Advances and the discovery opens the possibility of designing new types of drugs against conditions such as epilepsy.