Contribution of GABA(B) receptor-mediated inhibition to the expression and termination of group I mGluR-induced ictaform bursts

Epilepsy Res. 2004 Sep-Oct;61(1-3):161-5. doi: 10.1016/j.eplepsyres.2004.07.008.

Abstract

In guinea pig hippocampal slices, the GABA(B) receptor antagonist CGP 35348 increased the length of picrotoxin-induced interictal bursts by only 22%, yet it increased the length of group I mGluR-induced ictaform bursts by 85%. These data suggest that (1) suppression of GABAergic inhibition is insufficient to account for group I mGluR agonist-induced ictaform bursts, and (2) although GABA(B) plays a minor role in terminating interictal bursts, it is a major contributor to the termination of mGluR-induced ictaform bursts.

Publication types

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

MeSH terms

  • Animals
  • Convulsants / pharmacology
  • Electroencephalography / drug effects
  • Epilepsy / chemically induced
  • Epilepsy / physiopathology
  • GABA Antagonists / pharmacology
  • Glycine / analogs & derivatives*
  • Glycine / pharmacology
  • Guinea Pigs
  • In Vitro Techniques
  • Membrane Potentials / drug effects
  • Organophosphorus Compounds / pharmacology
  • Picrotoxin / pharmacology
  • Pyramidal Cells / drug effects
  • Pyramidal Cells / physiology
  • Receptors, GABA-B / drug effects
  • Receptors, GABA-B / physiology*
  • Receptors, Metabotropic Glutamate / agonists*
  • Resorcinols / pharmacology

Substances

  • Convulsants
  • GABA Antagonists
  • Organophosphorus Compounds
  • Receptors, GABA-B
  • Receptors, Metabotropic Glutamate
  • Resorcinols
  • metabotropic glutamate receptor type 1
  • Picrotoxin
  • 3,5-dihydroxyphenylglycine
  • CGP 35348
  • Glycine