- Poster presentation
- Open Access
Effects of astrocytic mechanisms on neuronal hyperexcitability
© Grigorovsky and Bardakjian; licensee BioMed Central Ltd. 2014
- Published: 21 July 2014
- Glial Cell
- Spike Train
- Neuronal Spike
- Neuronal Hyperexcitability
- Rectify Potassium Channel
Epileptic seizures affect one in hundred people and about 30% of all patients don’t benefit from medication and have to rely on other intervention methods. Current computer models of epilepsy frequently focus on neurons and their interactions to explain both the normal and pathological events in the brain. Recent research has linked glial cell to various cellular processes that are necessary for signal generation and propagation . Several mechanisms by which glial cells could influence the rest of the network have been proposed. One mechanism is the effect of potassium clearance on maintaining homeostatic ion concentration in the extracellular matrix which, when impaired, could lead to seizure-like activity . In addition to directly affecting potassium concentration in the extracellular space (ECS), impaired astrocytes become unable to maintain acceptable intracellular chloride concentrations in the neurons, which can cause or extend seizure-like events .
We introduce a computational model of CA3 region of hippocampus, consisting of a network of an astrocyte and a pyramidal cell with a feedback inhibited interneuron, to investigate the effects of a) potassium clearance and buffering by glial cells, and b) calcium propagation on neuronal hyperexcitability. Each cell was represented using modified Traub’s compartment models . Glial contribution was split into two separate factors – K+ clearance and buffering, partially revised from Oyehaug  and calcium interactions.
We would like to acknowledge Canadian Institutes for Health Research (CIHR) for providing the opportunity to investigate neuron-glia interactions under hyperexcitable conditions.
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