Absence seizures occur in many types of epilepsy but they are not well understood. In absence seizures, epileptic activity arises in the thalamus (which relays messages from our senses) and the cortex (the outermost layer of the brain). This study will investigate the mechanisms of how these seizures happen, focusing particularly on the principal inhibitory messenger chemical in the brain, GABA, and its activity in the thalamus and cortex. GABA carries messages from neurone to neurone via receptors at their synapses (the linking points at the end of their long arms). However, GABA is also involved in a recently-discovered type of communication between neurones called “tonic inhibition”. This is a constant background drift of the inhibitory neurotransmitter to receptors located outside the synapses. This slows the cells’ rate of communicating. Dr David Cope, of School of Biosciences, Cardiff University has shown that this type of inhibition is doubled in brain tissue from the thalamus affected by absence seizures. This means there has been a change in the number of receptors that can interact with GABA in this way. It’s not yet clear how widespread these changes are, or exactly how they lead to seizures. Dr Cope will investigate whether similar changes also occur in cortex cells affected by absence seizures, and also to look at the mechanisms that cause these changes. His 3-year study is called Extrasynaptic GABAA receptor-mediated gain-of-function in absence seizures. Dr Cope hopes his work will improve our understanding of how absence seizures happen, leading potentially to new ways of tackling them with drugs, and also to the identification of genes that can cause this type of seizures.