Astrocytic function and its alteration in the epileptic brain.
Currently available anticonvulsant drugs and complementary therapies are insufficient to control seizures in about a third of epileptic patients. Thus, there is an urgent need for new treatments that prevent the development of epilepsy and control it better in patients already afflicted with the disease. A prerequisite to reach this goal is a deeper understanding of the cellular basis of hyperexcitability and synchronization in the affected tissue. Epilepsy is often accompanied by massive reactive gliosis. Although the significance of this alteration is poorly understood, recent findings suggest that modified astroglial function may have a role in the generation and spread of seizure activity. Here we summarize properties of astrocytes as well as their changes that can be associated with epileptic tissue. The goal is to provide an understanding of the current knowledge of these cells with the long-term view of providing a foundation for the development of novel hypotheses about the role of glia in epilepsy.
Jabs
Ronald
R
Institute of Cellular Neurosciences, Medical Faculty, University of Bonn, Bonn, Germany.
Seifert
Gerald
G
Steinhäuser
Christian
C
D027322:Amino Acid Transport System X-AG / Q000502:physiology; D020346:Aquaporins / Q000502:physiology; D001253:Astrocytes / Q000502:physiology*; D001921:Brain / Q000166:cytology / Q000503:physiopathology*; D015220:Calcium Channels / Q000502:physiology; D020013:Calcium Signaling / Q000502:physiology; D004827:Epilepsy / Q000503:physiopathology*; D004833:Epilepsy, Temporal Lobe / Q000503:physiopathology; D005911:Gliosis / Q000503:physiopathology*; D006801:Humans; D008959:Models, Neurological; D015221:Potassium Channels / Q000502:physiology; D017470:Receptors, Glutamate / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology
D027322:Amino Acid Transport System X-AG; D020346:Aquaporins; D015220:Calcium Channels; D015221:Potassium Channels; D017470:Receptors, Glutamate; D015222:Sodium Channels