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Overview Article Astrocytes as Initiators of Epilepsy

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Summary: This study identified significantly reduced levels of claudin-5 protein in the brain tissue of epilepsy patients, and disruption of claudin-5 exacerbates epilepsy symptoms and BBB dysfunction in mice. Additionally, RepSox and other drugs targeting claudin-5 expression showed potential in preventing seizure activity in experimental epilepsy.

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Summary: Changes in astrocyte channels, transporters, and metabolism are closely linked to seizure generation and epilepsy, with alterations in potassium, glutamate, water and adenosine homeostasis contributing to hyperexcitability and epileptogenesis. Understanding the role of astrocytes in epilepsy offers potential for identifying novel astrocyte-specific therapeutic targets.

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Summary: Experimental models of epilepsy, particularly the kainic acid model, offer researchers a rich variety of phenotypes that can help in understanding the mechanisms and potential treatments of temporal lobe epilepsy. The different modes of KA administration produce varied effects and outcomes, highlighting the importance of considering strain, species, gender, and age factors in research. Additional work is needed to fully explore the potential of KA models in epilepsy research.

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