Effect of gamma-vinyl gamma-aminobutyric acid on the gamma-aminobutyric acid receptor-coupled chloride ion channel in vesicles from the brain of the rat

Neuropharmacology. 1991 May;30(5):423-7. doi: 10.1016/0028-3908(91)90002-s.

Abstract

The effect of gamma-vinyl GABA on the gamma-aminobutyric acid (GABA) receptor-coupled chloride ion (Cl-) channel was studied using membrane vesicles from cerebral cortex of the rat. gamma-Vinyl GABA, an antiepileptic drug, had no effect on uptake of 36Cl-, without preincubation. However, preincubation of membrane vesicles with gamma-vinyl GABA (100-1000 microM) produced a concentration-dependent decrease in net uptake of 36Cl-. No alteration was observed in basal uptake of 36Cl-. This decrease in net uptake of 36Cl- was not related to desensitization induced by endogenous GABA, which might be increased by gamma-vinyl GABA through selective, irreversible inhibition of GABA-transaminase (GABA-T). Concentration-response curves for GABA showed that preincubation with gamma-vinyl GABA inhibited GABA-stimulated uptake of 36Cl- with no change in ED50. These results indicate that gamma-vinyl GABA may act directly at the GABA/benzodiazepine ionophore complex, as a non-competitive antagonist of GABA.

MeSH terms

  • 4-Aminobutyrate Transaminase / antagonists & inhibitors*
  • Aminocaproates / pharmacology*
  • Animals
  • Brain / metabolism*
  • Chloride Channels
  • Chlorides / metabolism*
  • In Vitro Techniques
  • Ions
  • Male
  • Membrane Proteins / metabolism*
  • Membranes / metabolism
  • Rats
  • Rats, Inbred Strains
  • Receptors, GABA-A / drug effects*
  • Time Factors
  • Vigabatrin

Substances

  • Aminocaproates
  • Chloride Channels
  • Chlorides
  • Ions
  • Membrane Proteins
  • Receptors, GABA-A
  • 4-Aminobutyrate Transaminase
  • Vigabatrin