Epilepsy is a common chronic neurological disorder affecting more than 1% of the population. Epileptic seizures are uncontrolled sudden attacks of a convulsive or non-convulsive nature, associated with intense neuronal firing. The cellular mechanisms underlying seizure activity are incompletely understood, therefore hindering current medical management. Unfortunately, few novel treatments for the prevention of Traumatic brain injury (TBI)-induced seizures have been developed over the past century. TBI is a leading cause for seizures, which offers a good model for studying the mechanism behind epilepsy. TBI patients may exhibit seizures within a week or following several years after injury, both cases being related to the severity of TBI. Furthermore, mechanisms for acute and chronic seizures may differ, as inflammation-induced factors play an important role in acute seizure, whereas a spatially restricted seizure focus in the brain can often be identified for chronic seizure. Astrocytes, star-shaped glial cells, have been associated with seizure activity and are organized into these spatial domains.
Multiple lines of evidence support the contribution of astrocytes for both acute and chronic TBI-induced seizure. Astrocytes are the most numerous glial cell type and account for one third of brain mass. Historically, glial cells were thought to provide only metabolic and physical support for neurons, serving as the primary source of energy for neurons and serving to control ionic homeostasis and neuronal excitability by buffering K+. Current research has expanded our knowledge and found that astrocytes can actively regulate these processes, activated by agonist-induced Ca2+ waves. Astrocytes are also actively involved in the maintenance of the blood-brain barrier, regulating water and ion homeostasis and amino acid neurotransmitter metabolism, as well as energy and nutrient support of neurons. Many properties of astrocytes also make them important targets for the developing field of epilepsy treatment, and significant advances have been made in epilepsy research in the last decades.
In this Research Topic, we welcome research studies exploring the role of astrocytes in TBI-induced seizures. We welcome the following submission formats: original quantitative or qualitative research, review articles, perspectives, and case studies. The themes may include but are not limited to the following:
1. The relationship of the astrocytes and TBI-induced seizures.
2. The molecular mechanisms that activate astrocytes during TBI or spinal cord injury.
3. The functional changes of astrocytes at TBI occurrence, including buffering ability or extracellular space changes.
4. Glymphatic changes after TBI, and its role in TBI-induced seizures.
5. Epigenetic or protein expression alterations for astrocytes and neurons, such as NKCC1, Kir4.1.
6. Drugs that affect astrocytes or neurons after neuronal injury.
7. The interactions between astrocytes and inhibitory neurons at neuronal injury.
Epilepsy is a common chronic neurological disorder affecting more than 1% of the population. Epileptic seizures are uncontrolled sudden attacks of a convulsive or non-convulsive nature, associated with intense neuronal firing. The cellular mechanisms underlying seizure activity are incompletely understood, therefore hindering current medical management. Unfortunately, few novel treatments for the prevention of Traumatic brain injury (TBI)-induced seizures have been developed over the past century. TBI is a leading cause for seizures, which offers a good model for studying the mechanism behind epilepsy. TBI patients may exhibit seizures within a week or following several years after injury, both cases being related to the severity of TBI. Furthermore, mechanisms for acute and chronic seizures may differ, as inflammation-induced factors play an important role in acute seizure, whereas a spatially restricted seizure focus in the brain can often be identified for chronic seizure. Astrocytes, star-shaped glial cells, have been associated with seizure activity and are organized into these spatial domains.
Multiple lines of evidence support the contribution of astrocytes for both acute and chronic TBI-induced seizure. Astrocytes are the most numerous glial cell type and account for one third of brain mass. Historically, glial cells were thought to provide only metabolic and physical support for neurons, serving as the primary source of energy for neurons and serving to control ionic homeostasis and neuronal excitability by buffering K+. Current research has expanded our knowledge and found that astrocytes can actively regulate these processes, activated by agonist-induced Ca2+ waves. Astrocytes are also actively involved in the maintenance of the blood-brain barrier, regulating water and ion homeostasis and amino acid neurotransmitter metabolism, as well as energy and nutrient support of neurons. Many properties of astrocytes also make them important targets for the developing field of epilepsy treatment, and significant advances have been made in epilepsy research in the last decades.
In this Research Topic, we welcome research studies exploring the role of astrocytes in TBI-induced seizures. We welcome the following submission formats: original quantitative or qualitative research, review articles, perspectives, and case studies. The themes may include but are not limited to the following:
1. The relationship of the astrocytes and TBI-induced seizures.
2. The molecular mechanisms that activate astrocytes during TBI or spinal cord injury.
3. The functional changes of astrocytes at TBI occurrence, including buffering ability or extracellular space changes.
4. Glymphatic changes after TBI, and its role in TBI-induced seizures.
5. Epigenetic or protein expression alterations for astrocytes and neurons, such as NKCC1, Kir4.1.
6. Drugs that affect astrocytes or neurons after neuronal injury.
7. The interactions between astrocytes and inhibitory neurons at neuronal injury.
