A burst-dependent hippocampal excitability defect elicited by potassium at the developmental onset of spike-wave seizures in the Tottering mutant. Academic Article uri icon

Overview

abstract

  • Hippocampal CA3 pyramidal neurons in the adult epileptic mutant mouse tottering (tg) show normal intrinsic membrane properties, yet fire abnormally prolonged paroxysmal depolarizing shifts (PDS) during in vitro exposure to elevated extracellular potassium solutions. Intracellular recordings in immature mutants reveal that this network burst abnormality is present during the developmental period that coincides with the onset of seizures in the mutant (19-20 postnatal days), and is significantly more pronounced at this age than at adulthood. These data are inconsistent with the hypothesis that the mutant PDS prolongation represents a secondary consequence of a prolonged history of repeated seizures and suggest that it may reflect a cellular epileptogenic phenotype more directly related to the primary neuropathological expression of the tg gene.

publication date

  • February 21, 1992

Research

keywords

  • Hippocampus
  • Potassium
  • Seizures

Identity

Scopus Document Identifier

  • 0026568246

Digital Object Identifier (DOI)

  • 10.1016/0165-3806(92)90180-5

PubMed ID

  • 1572065

Additional Document Info

volume

  • 65

issue

  • 2