Grant winner 2017

‘Absence epilepsy is a childhood form of epilepsy, in which there are sudden and brief interruptions of consciousness. If these happen frequently enough they can interfere with learning and can lead to convulsions. We plan to investigate the role that glial cells play in this condition. We hypothesize that deficits in one particular form of glial cell signalling (purinergic) could lead to the enhanced synaptic inhibition that underlies absence episodes. Our work will hopefully identify a new therapeutic target to treat absence epilepsy and increase understanding of the disease.Dr Mark Wall (pictured)

Grant type: Pilot grant

Principal investigator: Dr Mark Wall

Institution: University of Warwick

Amount: £29,300

Duration: 18 months

Scientific title: The role of gliotransmission in absence epilepsy

Background
Absence epilepsy is largely a childhood condition characterised by sudden, brief interruptions of consciousness. In severe cases there may be more than 200 of these episodes each day, and these can be accompanied by or develop into convulsive seizures. Many children with absence seizures don’t respond to existing antiepileptic medication, which can present numerous difficulties in daily life, particularly with schooling.

On EEG, absence seizures show a specific pattern of brain activity that arises within a neuronal network called the thalamo-cortical network. The mechanisms that generate these episodes are still not fully understood, but evidence shows that enhancement of a particular type of inhibitory communication between neurons may be responsible. Attempts to develop treatments that directly reduce this inhibition have failed because of side effects, so a more targeted approach is required.

The Study
This grant focuses on brain cells called glial cells, which support neurons and are important for maintaining correct communication between them. More specifically, Dr Wall and Dr Richard Ngomba (University of Lincoln) want to find out if a loss of glial cell function is responsible for the increased inhibition that leads to absence seizures.

The group will use a range of laboratory techniques to explore, in depth, how certain aspects of glial activity are altered in a rodent model of absence epilepsy. They also plan to investigate whether it is possible to reduce or even prevent absence seizures by enhancing glial cell activity.

Significance
The findings from this project will give important new information about how absence seizures arise, and may reveal new targets for the development of more promising treatments. The methods used will also be useful for the screening process of anti-absence seizure drugs in the future.

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