Abstract
Based on recent experimental data, we design a model for neuronal membrane potentials that incorporates the influence of the surrounding glia (dressed neurons). A neurotransmitter released into the synaptic cleft triggers a Ca2+ response in nearby glial cells that spreads as a Ca2+ wave and interacts with other synapses via the release of glutamate from astrocytes. We consider the simple case of a neuron–glia circuit that consists of a single neuron that triggers a Ca2+ response in the glial cell which in turn feeds back into synapses of the same neuron. It is shown that persistent spiking can occur if the glutamate receptors on the astrocytes are overexpressed—a condition that has been reported from patients suffering from mesial-lobe epilepsy.
Published Version
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