Enhancement of GABA-mediated postsynaptic inhibition in cultured mammalian spinal cord neurons: a common mode of anticonvulsant action

Brain Res. 1979 May 11;167(2):323-36. doi: 10.1016/0006-8993(79)90826-6.

Abstract

Murine spinal cord neurons grown in dissociated cell culture were used to study the effects of barbiturate (phenobarbital, mephobarbital) and benzodiazepine (diazepam, chlordiazepoxide( anticonvulsants on amino acid responses. Both types of anticonvulsant augmented GABA-mediated postsynaptic inhibition without augmenting beta-alanine or glycine-mediated postsynaptic inhibition. Barbiturates, but not benzodiazepines, antagonized glutamate-mediated postsynaptic excitation. Augmentation of GABA-mediated inhibition by the anticonvulsants should contribute to their anticonvulsant action; antagonism of glutamate-mediated excitation by barbiturates should also contribute to their anticonvulsant action and could be at least in part responsible for their sedative actions.

MeSH terms

  • Animals
  • Anticonvulsants / pharmacology*
  • Chlordiazepoxide / pharmacology
  • Culture Techniques
  • Diazepam / pharmacology
  • Evoked Potentials / drug effects
  • Glutamates / pharmacology
  • Mephobarbital / pharmacology
  • Mice
  • Neural Conduction / drug effects
  • Neural Inhibition / drug effects*
  • Neurons / drug effects
  • Penicillin G / pharmacology
  • Phenobarbital / pharmacology
  • Spinal Cord / drug effects*
  • Synapses / drug effects*
  • gamma-Aminobutyric Acid / pharmacology*

Substances

  • Anticonvulsants
  • Glutamates
  • gamma-Aminobutyric Acid
  • Mephobarbital
  • Chlordiazepoxide
  • Diazepam
  • Penicillin G
  • Phenobarbital