Pathological Changes of Astrocytes under Seizure

Shanshan Lu

doi:10.23937/2469-5866/1510008

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

Highlights

Epilepsy is a common chronic neurologic disorder affecting at least 50 million people [1,2], or more than 1% of the population worldwide [3,4,5]
The present review summarized the roles of reactive astrocytes in the development and progression of epileptic seizures, and discussed the relevance of calcium signaling in astrocytes to therapeutic management of the disease
Epilepsy is a common chronic neurologic disorder affecting ~1% of the population with an estimated lifetime risk greater than 4%

Summary

Introduction

Epilepsy is a common chronic neurologic disorder affecting at least 50 million people [1,2], or more than 1% of the population worldwide [3,4,5]. Astrocytes are involved in regulating ion homeostasis, maintenance of the blood brain barrier (BBB) function, metabolism of amino acid neurotransmitter, as well as nutrient and energy support for neurons [12]. The mechanisms of glial scar inducing seizure are possibly due to astrogliosis, with its ability of K+ buffering and neurotransmitter clear up decreased.

Results

Conclusion