The Max Planck scientists were also the first to successfully prove the third hypothesis that the nerve cells of mice with a genetic ClC-2 deficiency were much easier to excite than nerve cells in a healthy brain. Earlier assumptions therefore turned out to be correct. Then why did animals lacking the ClC-2 channels show no sign of epilepsy?
The answer to this question was not only plausible, but also straightforward. In addition to having cells that transmit information to their neighbouring cells, the nervous system contains a second group of nerve cells. These cells inhibit the exchange of information between its neighbours. In animals with a ClC-2 genetic defect, these inhibitory nerve cells also forfeit their chloride channels, and therefore become more excitable. Thus, excitatory and inhibitory cells become more excitable. "Although the whole system becomes more sensitive, at the end of the day the balance between the cells is maintained", explains Valentin Stein, leader of the study. And so the anticipated connection between genetic defect and epilepsy is not expressed. However, the lack of ClC-2 channels throws the nervous system into an unnaturally excited state. The scientists therefore speculate that although a defective ClC-2 gene does not cause epilepsy in itself, it may increase the risk of contracting epilepsy if other factors are present.
"We reckon, however, that we have come across something even more exciting", says Valentin Stein . The neurobiologist is referring to the discovery that nerve cells can theoretically use the ClC-2 channels to influence their own excitability. "If a nerve cell can control its own excitability by opening or closing its ClC-2 channels, then it could basically have a say in whether or not it transmits information to its neighbour." This possibility adds a whole new d
|Contact: Valentin Stein|