Abstract
Traumatic brain injury, a common cause of acquired epilepsy, is typical to find necrotic cell death within the injury core. The dynamic changes in astrocytes surrounding the injury core contribute to epileptic seizures associated with intense neuronal firing. However, little is known about the molecular mechanisms that activate astrocytes during traumatic brain injury or the effect of functional changes of astrocytes on seizures. In this comprehensive review, we present our cumulated understanding of the complex neurological affection in astrocytes after traumatic brain injury. We approached the problem through describing the changes of cell morphology, neurotransmitters, biochemistry, and cytokines in astrocytes during post-traumatic epilepsy. In addition, we also discussed the relationship between dynamic changes in astrocytes and seizures and the current pharmacologic agents used for treatment. Hopefully, this review will provide a more detailed knowledge from which better therapeutic strategies can be developed to treat post-traumatic epilepsy.
Highlights
Astrocytes, star-shaped glial cells, constitute ∼30% of cells in the central nervous system (CNS) [1]
It is clear that astrocytes are key players in the epileptogenesis induced by traumatic brain injury
A number of astrocytespecific functions linked to post-traumatic epilepsy have been affected, such as cytokine regulation, water regulation, neurotransmitters and ion homeostasis, and blood–brain barrier maintenance (Figure 2)
Summary
Astrocytes, star-shaped glial cells, constitute ∼30% of cells in the central nervous system (CNS) [1] They are tightly integrated into neural networks and provide metabolic and physical support for neurons [2]. The extensions enwrap of astrocytes with presynaptic terminals and post-synaptic spines generate a complex, interconnected hub, the so-called tripartite synapse [7]. This may be the dominant form of astrocyte–neuron interactions. In this context, astrocytes have been implicated in the etiology of epileptic seizures. We clarify the interaction between post-traumatic epilepsy and astrocytes
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