Cellular mechanisms underlying absence epilepsy

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Absence epilepsy is the commonest form of idiopathic generalized epilepsy. It can lead to hundreds of seizures per day, and mainly affects children between the ages of four and eight. Its cause is in most cases unknown. In this study we will use a rat model of absence epilepsy to investigate the cellular basis of this disease. Preliminary work indicates that a particular protein - HCN1 - is reduced in the cortex of rats with absence epilepsy. This protein codes for a pore in the membrane of nerve cells, which acts like a switch. We have preliminary evidence that in rats with absence epilepsy this switch does not work properly. We wish to investigate how this influences the activity of nerve cells in rats with absence epilepsy. Furthermore, as absence epilepsy is an inherited disease, we wish to track down the genetic basis of this disease. This will give us clues as to the cause of the disease in this rat model. This research will shed light on the potentially important role of the HCN1 protein in absence epilepsy, which may represent an potentially new therapeutic target for the development of drugs for the treatment of absence epilepsy.