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NBQX or Topiramate Treatment after Perinatal Hypoxia‐induced Seizures Prevents Later Increases in Seizure‐induced Neuronal Injury
Author(s) -
Koh Sookyong,
Tibayan Felicia D.,
Simpson Joelle N.,
Jensen Frances E.
Publication year - 2004
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.0013-9580.2004.69103.x
Subject(s) - nbqx , hypoxia (environmental) , seizure threshold , anticonvulsant , anesthesia , ampa receptor , epilepsy , topiramate , medicine , pharmacology , nmda receptor , chemistry , receptor , oxygen , organic chemistry , psychiatry
Summary: Purpose: To evaluate the efficacy of NBQX (2,3‐dihydroxy‐6‐nitro‐7‐sulfamoylbenzo(f) quinoxaline‐2,3‐dione) and topiramate (TPM) given after hypoxia‐induced seizures in preventing the delayed effect of hypoxia on subsequent susceptibility to seizures and neuronal injury. Methods: We used “two‐hit” rodent seizure model to study the long‐term effect of perinatal hypoxia on later kainate (KA) seizure‐induced neuronal damage and investigated the therapeutic efficacy of a postseizure treatment protocol in reversing the conditioning effect of early‐life seizures. Results: Hypoxia at P10 induces seizures without cell death but causes an increase in susceptibility to second seizures induced by KA as early as 96 h after hypoxia, and this lowered seizure threshold persists to adulthood. Furthermore, perinatal hypoxia increases KA‐induced neuronal injury at postnatal day (P)21 and 28/30. Repeated doses of NBQX (20 mg/kg) or TPM (30 mg/kg) given for 48 h after hypoxia‐induced seizures prevent the increase in susceptibility to KA seizure‐induced hippocampal neuronal injury at P28/30. Conclusions: Our results suggest that α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptor blockade after hypoxia prevents the priming effect of perinatal hypoxia‐induced seizures and that this protection occurs independent of its anticonvulsant action.