Through ion chanells

Jan 25, 2007 10:55 GMT  ·  By

The 100 billion nerve cells composing our brains form a web crossed all the time by electrical signals.

These neurons, in turn, not only communicate between them but also coordinate the organs in the body.

But how do the neurons manage the whole cascades of responses, which are highly specific, quick and precisely timed? A research at the Weizmann Institute of Science has explained some of the unknown mechanisms, with an importance for the future synthesis of drugs for epilepsy and other nervous system diseases.

The electrical signals generated by cells depend on ion channels, proteins situated in the neuronal membrane, which trigger the electrical signals, depending on whether the channels are opened or closed.

The research team led by Professor Eitan Reuveny focused on potassium ions and the correspondent G protein, which - when activated - causes the channel to open. Opening the channel stops the conductance of electrical signals, a relevant factor in fighting against epilepsy seizures. The G protein itself is turned on by another protein, named receptor, which receives the signal to carry out its task from messenger molecules named neurotransmitters. But neurotransmitters can inhibit as well as excite, and the receptors can make the difference to either message.

The researchers, focusing on understanding how the G protein receives so quickly and precisely the message to activate the channel, discovered that the receptor and G protein form a physical bound, tuning finely the process. When the receptor picks up a message from the neurotransmitter, it is already fixed up to the right G protein, which will open the ion channel.

The FRET (Fluorescence Resonance Energy Transfer) technology enabled the investigators to measure the distance between two molecules. They noticed that even without stimulation, there is an energy change between the G protein and the potassium channel, pointing to the fact that they are very close together. Impairments in ion channels due to mutations may be behind epilepsy, chronic pain, neurodegenerative diseases and muscular diseases. Understanding these processes will enhance the design of better or more efficient drugs.