Researchers at the University of Bonn have made a significant breakthrough in understanding the primary trigger behind the onset of temporal lobe epilepsy. The genesis lies in the early-stage malfunctioning of astrocytes, a type of brain cell. It leads to the uncoupling of astrocytic processes from each other, subsequently giving rise to the accumulation of potassium ions and neurotransmitters outside the cells, which in turn, leads to an excessive excitation of neurons, which is a hallmark of epilepsy.
Astrocytes, the star-shaped cells in the brain, are typically interconnected through specialized channels called gap junctions. These gap junctions predominantly consist of two types of proteins: connexin 43 and connexin 30. Employing a combination of patch-clamp recordings and diverse immunotechniques, the scientists in this study delved into the precise role of impaired gap junction channels in the development of epilepsy.
The findings underscore the crucial importance of addressing astrocyte dysfunction in order to combat epilepsy effectively. By rectifying the malfunctioning gap junction channels and restoring the connectivity between astrocytes, an avenue for potential therapeutic intervention against epilepsy emerges. This innovative strategy of targeting the root cause of the disorder marks a promising direction for future anti-epileptogenic treatments.
Bedner P, Dupper A, Hüttmann K, Müller J, Herde MK, Dublin P, Deshpande T, Schramm J, Häussler U, Haas CA, Henneberger C, Theis M, & Steinhäuser C (2015). Astrocyte uncoupling as a cause of human temporal lobe epilepsy. Brain : a journal of neurology, 138 (Pt 5), 1208-22 PMID: 25765328






Scientists at the 