Nerve cells communicate with each other by means of electrical impulses. To create such an impulse, the cells exchange charged ions with their environment. However, the role played by the ever-present chloride channels remained obscure, although some theories predicted a relation between the chloride channel ClC-2 and epilepsy. Scientists at the Max Planck Institute of Neurobiology in Martinsried were now able to confirm a number of assumptions about the ClC-2 channel and could at last explain why the anticipated epileptic seizures do not occur when nerve cells lack the ClC-2 channels in mice. The results also provide a completely new understanding of how nerve cells may actively influence the exchange of information. (The Journal of Neuroscience online publication 01 April 2010)
The cell membranes of nerve cells, like those of all other cell types in the body, are perforated by so-called chloride channels. These permit the exchange of negatively charged chloride ions between the cell and its environment. Yet scientists could so far only speculate about the purpose of this exchange. According to one very prevalent theory, the excitability of nerve cells decreases when they lose chloride ions through these channels. Or, to put it the other way round, the lack of chloride channels would cause nerve cells to become overexcited. This in turn should lead to an increased rate of epileptic seizures. However, mice whose nerve cells lack chloride channels due to a genetic mutation were found no more susceptible to epilepsy than healthy animals. And so the function of the ClC-2 and of other chloride channels remained obscure.
Scientists at the Max Planck Institute of Neurobiology have now tracked down a number of the ClC-2 channel's functions. This constitutes the first tangible proof of the circumstances under which chloride ions can escape from nerve cells through the ClC-2 channels. In the case that nerve cells were lacking the ClC-2 chan
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