The neonatal period represents one of the highest incidence periods for seizures across the lifespan. Hypoxic and/or ischemic encephalopathy is the most common cause for neonatal seizures, and accounts for more than two-thirds of neonatal seizure cases. Patients with neonatal seizures are often refractory to conventional antiepileptic drugs, and can result in later life epilepsy and cognitive deficits, conditions for which there are no specific treatments. A better understanding of the cellular and molecular mechanisms is essential for identifying new therapeutic strategies that control the neonatal seizures and its long-term cognitive comorbidities. In this regard, animal models play an essential role in discovering novel mechanisms underlying both epileptogenesis and associated cognitive comorbidities. To date, a number of animal models have made tremendous progress in our understanding of the pathophysiology of HIE-induced neonatal seizures. This chapter provides an overview on the most important features of the main animal models of hypoxia-induced seizures in developing brain. In particular, we focus on the methodology of seizure induction and the characterizations of postseizure consequences. These aspects of hypoxia-induced seizure models are discussed in the light of the suitability of these models in studying human HIE-induced seizures.

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Keywords Cognitive comorbidities, Cortex, Epileptogenesis, Hippocampus, Hypoxia, Neonate
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Sun, H, & Jensen, F.E. (Frances E.). (2017). Modeling Hypoxia-Induced Seizures and Hypoxic Encephalopathy in Developing Brain. In Models of Seizures and Epilepsy: Second Edition (pp. 697–711). doi:10.1016/B978-0-12-804066-9.00048-1