Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits

Nat Med. 1999 Aug;5(8):888-94. doi: 10.1038/11330.

Abstract

Febrile (fever-induced) seizures affect 3-5% of infants and young children. Despite the high incidence of febrile seizures, their contribution to the development of epilepsy later in life has remained controversial. Combining a new rat model of complex febrile seizures and patch clamp techniques, we determined that hyperthermia-induced seizures in the immature rat cause a selective presynaptic increase in inhibitory synaptic transmission in the hippocampus that lasts into adulthood. The long-lasting nature of these potent alterations in synaptic communication after febrile seizures does not support the prevalent view of the 'benign' nature of early-life febrile convulsions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Brain / growth & development
  • Brain / physiopathology*
  • Culture Techniques
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / physiology
  • Enzyme Inhibitors / pharmacology
  • Evoked Potentials / drug effects
  • Evoked Potentials / physiology
  • Hypothalamus / physiology
  • Limbic System / physiopathology*
  • Neural Inhibition / drug effects
  • Neural Inhibition / physiology
  • Neuronal Plasticity / physiology*
  • Patch-Clamp Techniques
  • Presynaptic Terminals / physiology
  • Pyramidal Cells / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Seizures, Febrile / physiopathology*
  • Synaptic Transmission / physiology

Substances

  • Enzyme Inhibitors
  • Cyclic AMP-Dependent Protein Kinases