Abstract

Multiple lines of studies support the view that defective functions of astrocytes contribute to neuronal hyper-excitability in the epileptic brain. Autopsy and surgical resection specimens find that post-traumatic seizures and chronic temporal lobe epilepsy may originate from glial scars. Astrogliosis, a component of glial scar, which involves structural and metabolic changes in astrocytes, is often a prominent feature of temporal epilepsy and most animal models of recurrent seizures. Although glial scar formation has been recognized for over 120 years, fundamental aspects of the cellular mechanisms are poorly understood. We here provide an overview of the experimental findings about astrogliosis in seizures, which involves the changes in astrocytic structure and loss of domain. These structure changes are paralleled by functional changes, including expression levels of glutamate transporter and glutamine synthetase. Reactive astrocytes have also been shown to down-regulate the activities of K+ channels, leading to impairment of clearance of K+. The functional remodeling may contribute to increased neuronal excitability and generation of seizures.

Authors and Affiliations