Astroglial role in the pathophysiology of status epilepticus: an overview

Rodrigo Esteban Gonzalez Reyes, Karina Vargas-Sánchez, Maria Mogilevskaya, John Rodríguez-Pérez, María Graciela Rubiano, José Julián Javela

Research output: Contribution to journalReview article

5 Citations (Scopus)

Abstract

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.
Original languageEnglish (US)
Pages (from-to)26954-26976
JournalOncotarget
Volume9
DOIs
StatePublished - Jun 1 2018

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Status Epilepticus
Astrocytes
Neuroglia
Seizures
Central Nervous System
Gap Junctions
Extracellular Space
Glutamic Acid
Epilepsy
Reactive Oxygen Species
Emergencies
Maintenance
Cytokines
Inflammation
Morbidity
Neurons
Mortality
Research

Cite this

Gonzalez Reyes, R. E., Vargas-Sánchez, K., Mogilevskaya, M., Rodríguez-Pérez, J., Rubiano, M. G., & Javela, J. J. (2018). Astroglial role in the pathophysiology of status epilepticus: an overview. Oncotarget, 9, 26954-26976. https://doi.org/10.18632/oncotarget.25485
Gonzalez Reyes, Rodrigo Esteban ; Vargas-Sánchez, Karina ; Mogilevskaya, Maria ; Rodríguez-Pérez, John ; Rubiano, María Graciela ; Javela, José Julián. / Astroglial role in the pathophysiology of status epilepticus: an overview. In: Oncotarget. 2018 ; Vol. 9. pp. 26954-26976.
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Gonzalez Reyes, RE, Vargas-Sánchez, K, Mogilevskaya, M, Rodríguez-Pérez, J, Rubiano, MG & Javela, JJ 2018, 'Astroglial role in the pathophysiology of status epilepticus: an overview', Oncotarget, vol. 9, pp. 26954-26976. https://doi.org/10.18632/oncotarget.25485

Astroglial role in the pathophysiology of status epilepticus: an overview. / Gonzalez Reyes, Rodrigo Esteban; Vargas-Sánchez, Karina; Mogilevskaya, Maria; Rodríguez-Pérez, John; Rubiano, María Graciela; Javela, José Julián.

In: Oncotarget, Vol. 9, 01.06.2018, p. 26954-26976.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Astroglial role in the pathophysiology of status epilepticus: an overview

AU - Gonzalez Reyes, Rodrigo Esteban

AU - Vargas-Sánchez, Karina

AU - Mogilevskaya, Maria

AU - Rodríguez-Pérez, John

AU - Rubiano, María Graciela

AU - Javela, José Julián

PY - 2018/6/1

Y1 - 2018/6/1

N2 - 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.

AB - 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.

U2 - 10.18632/oncotarget.25485

DO - 10.18632/oncotarget.25485

M3 - Review article

VL - 9

SP - 26954

EP - 26976

JO - Oncotarget

JF - Oncotarget

SN - 1949-2553

ER -

Gonzalez Reyes RE, Vargas-Sánchez K, Mogilevskaya M, Rodríguez-Pérez J, Rubiano MG, Javela JJ. Astroglial role in the pathophysiology of status epilepticus: an overview. Oncotarget. 2018 Jun 1;9:26954-26976. https://doi.org/10.18632/oncotarget.25485