Absence epilepsy is a common epilepsy syndrome, which usually develops between the ages of four and nine years of age. Seizures can occur between 20 and several hundred times per day, and usually last between five and 20 seconds. During a seizure the person will briefly lose consciousness, stop whatever they are doing and stare blankly into space. They will be completely unaware of their surroundings and may show repetitive movements such as lip smacking of eye fluttering.

Neuronal pathways, known as thalamocortical circuits, exist between the thalamus (found in the centre of the brain) and the cortex (the folded surface of the brain). These pathways have an important role in normal sleep production, but they have also been found to be vital in the generation of absence seizures. Thus absence seizures may arise from a distortion of normal electrical activity within thalamocortical ‘sleep-wake’ circuits.

Cells in the thalamus that release the inhibitory neurotransmitter GABA play a pivotal role thalamocortical circuits. By acting on two different types of receptor, GABA can produce a mixture of short- and long-lived neuronal inhibition. However, it is not known how these separate types of inhibition interact to shape normal or abnormal behaviour (sleep or absence seizures respectively).

Dr Murray Herd, from the University of Dundee, has been awarded £197,531 over 36 months, to carry out a fellowship entitled Tonic and phasic GABAAR inhibition during thalamocortical network oscillations: relevance to absence epilepsy. He will use a variety of techniques to study the impact of GABA inhibition during states of sleep, wakefulness and absences, in order to increase our understanding of how alterations in the balance between short and long-lived inhibition (which would normally control sleep-wake cycles) may lead to absence seizures.

Dr Herd is hopeful that this research will lead to the development of more targeted and effective drugs for absence epilepsy in the future.