title: Enhanced long-term potentiation in mature rats in a model of epileptic spasms with betamethasone-priming and postnatal N-methyl-D-aspartate administration.
abstract: OBJECTIVE
  Patients with epileptic spasms are at high risk for learning and memory impairment later in life. We examined whether synaptic plasticity is affected in the adult hippocampus, a structure responsible for learning and memory, using an animal model of epileptic spasms of unknown cause.
  
  
  METHODS
  We produced a rat model of N-methyl-d-aspartate (NMDA)-induced spasms combined with prenatal betamethasone administration. In 6- to 11-week-old rats, we evaluated the long-term potentiation (LTP) and general properties of synaptic transmission in pyramidal neurons in the CA1 area of the hippocampus in brain slices.
  
  
  RESULTS
  The magnitude of LTP by theta burst stimulation was significantly larger in adult rats with a history of infantile NMDA injections than in control rats and rats that received additional adrenocorticotropic hormone (ACTH) treatment. The frequency of spontaneous excitatory transmission, but not inhibitory transmission, was smaller in adult rats with a history of infantile NMDA injections.
  
  
  CONCLUSIONS
  This study is the first to provide a basis for the alteration of synaptic plasticity and transmission in a model of epileptic spasms of unknown cause. Postnatal NMDA treatment causing epileptic spasms-like aberrant episodes in the early stage of life in rats has a latent influence on various forms of synaptic plasticity in the hippocampus. Our results provide a novel insight into cognitive impairment that appears later in life in patients with a history of epileptic spasms.
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Tokyo, Japan.|Division of Pediatric Neurology, Kanagawa Children's Medical Center, Yokohama, Japan.
authors.forename: Megumi
authors.initials: M
authors.lastname: Tsuji
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Tokyo, Japan.
authors.forename: Yukari
authors.initials: Y
authors.lastname: Takahashi
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Tokyo, Japan.|Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency, Kawaguchi, Saitama, Japan.
authors.forename: Ayako M
authors.initials: AM
authors.lastname: Watabe
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Tokyo, Japan.
authors.forename: Fusao
authors.identifier: http://orcid.org/0000-0003-0031-9946
authors.initials: F
authors.lastname: Kato
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001623:Betamethasone / Q000008:administration & dosage / Q000633:toxicity*; D004195:Disease Models, Animal; D004827:Epilepsy / Q000139:chemically induced* / Q000503:physiopathology*; D005260:Female; D017774:Long-Term Potentiation / Q000187:drug effects* / Q000502:physiology; D008297:Male; D016202:N-Methylaspartate / Q000008:administration & dosage / Q000633:toxicity*; D009924:Organ Culture Techniques; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016202:N-Methylaspartate; D001623:Betamethasone
keywords: Animal model; Epileptic spasms; Hippocampus; Long-term potentiation; Prenatal stress; Synaptic plasticity