Effects of astrocytic mechanisms on neuronal hyperexcitability

While originally astrocytes have been thought to only act as support to neurons, recent studies have implicated them in multiple active roles, including the ability to moderate or alter neuronal firing patterns and to possibly be involved in both the prevention and propagation of epileptic seizures. In this study we propose a new model to incorporate pyramidal cells and interneurons (a common neural circuit in CA3 hippocampal slices) as well as a model of astrocyte. As both potassium and calcium ions have been shown to potentially affect neuronal hyperexcitability, the astrocytic model has both mechanisms--the clearance of potassium through potassium channels (such as KIR, KDR and sodium-potassium pump), and the influence of astrocyte in the synapse (forming the tripartite synapse with calcium-glutamate interactions). Preliminary findings of the model results show that when potassium conductances in the astrocyte are decreased, it results in the accumulation of extracellular potassium, leading to both spontaneous discharges and depolarization block, while the alteration of normal calcium response in the astrocyte can lead to just hyperexcitable conditions without the depolarization block.