Does rapid and physiological astrocyte-neuron signalling amplify epileptic activity?
The hippocampus is a key brain region in the pathophysiology of mesial temporal lobe epilepsy. Long-term changes of its architecture and function on the network and cellular level are well documented in epilepsy. Astrocytes can control many aspects of neuronal function and their long-term alterations over weeks, months and years play an important role in epilepsy. However, a pathophysiological transformation of astrocytes does not seem to be required for astrocytes to contribute to epileptic activity. Some of the properties of physiological astrocyte-neuron communication could allow these cells to exacerbate or synchronize neuronal firing on shorter time scales of milliseconds to minutes. Therefore, these astrocyte-neuron interactions are increasingly recognized as potential contributors to epileptic activity. Fast and reciprocal communication between astrocytes and neurons is enabled by a diverse set of mechanisms that could both amplify and counteract epileptic activity. They may thus promote or cause development of epileptic activity or inhibit it. Mechanisms of astrocyte-neuron interactions that can quickly increase network excitability involve, for example, astrocyte Ca2+and Na+signalling, K+buffering, gap junction coupling and metabolism. However, rapid changes of astrocyte neurotransmitter uptake and morphology may also underlie or support development of network hyperexcitability. The temporal characteristics of these interactions, their ability to synchronize neuronal activity and their net effect on network activity will determine their contribution to the emergence or maintenance of epileptic activity.
Institute of Cellular Neurosciences, University of Bonn Medical School, Germany.|German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.|UCL Institute of Neurology, London, UK.
Christian
0000-0002-5391-7387
C
Henneberger
D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D004827:Epilepsy / Q000503:physiopathology*; D017629:Gap Junctions / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D015398:Signal Transduction; D012964:Sodium / Q000502:physiology
D012964:Sodium; D002118:Calcium