Astroglial role in the pathophysiology of status epilepticus: an overview
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Karina Vargas-Sánchez1, Maria Mogilevskaya2, John Rodríguez-Pérez1, María G. Rubiano1, José J. Javela3 and Rodrigo E. González-Reyes4
1Biomedical Sciences Research Group, School of Medicine, Universidad Antonio Nariño, Bogotá, Colombia
2Universidad ECCI, Bogotá, Colombia
3Grupo de Clínica y Salud Mental, Programa de Psicología, Universidad Católica de Pereira, Pereira, Colombia
4Universidad del Rosario, Escuela de Medicina y Ciencias de la Salud, GI en Neurociencias-NeURos, Bogotá, Colombia
Rodrigo E. González-Reyes, email: [email protected]
Keywords: astrocytes; status epilepticus; epilepsy; glia; neuroinflammation
Received: December 09, 2017 Accepted: May 09, 2018 Published: June 01, 2018
Status epilepticus is a medical emergency with elevated morbidity and mortality rates, and represents a leading cause of epilepsy-related deaths. Though status epilepticus can occur at any age, it manifests more likely in children and elderly people. Despite the common prevalence of epileptic disorders, a complete explanation for the mechanisms leading to development of self-limited or long lasting seizures (as in status epilepticus) are still lacking. Apart from neurons, research evidence suggests the involvement of immune and glial cells in epileptogenesis. Among glial cells, astrocytes represent an ideal target for the study of the pathophysiology of status epilepticus, due to their key role in homeostatic balance of the central nervous system. During status epilepticus, astroglial cells are activated by the presence of cytokines, damage associated molecular patterns and reactive oxygen species. The persistent activation of astrocytes leads to a decrease in glutamate clearance with a corresponding accumulation in the synaptic extracellular space, increasing the chance of neuronal excitotoxicity. Moreover, major alterations in astrocytic gap junction coupling, inflammation and receptor expression, facilitate the generation of seizures. Astrocytes are also involved in dysregulation of inhibitory transmission in the central nervous system and directly participate in ionic homeostatic alterations during status epilepticus. In the present review, we focus on the functional and structural changes in astrocytic activity that participate in the development and maintenance of status epilepticus, with special attention on concurrent inflammatory alterations. We also include potential astrocytic treatment targets for status epilepticus.
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