The effect of the experimental anticonvulsant, α-ethyl,methyl thiobutyrolactone (α-EMTBL), on γ-aminobutyric acid (GABA) currents was examined in cultured chick spinal cord neurons using gigaseal recording techniques. α-EMTBL potentiated GABA responses in a dose-dependent fashion with half-maximal effect at 7 μM. α-EMTBL also augmented the response to maximal doses of GABA. In competition experiments, α-EMTBL relieved the block of GABA currents produced by saturating concentrations of picrotoxinin whereas diazepam and phenobarbital did not. At a single channel level, α-EMTBL increased the probability of opening GABA channels without significantly altering the mean channel open time or the single channel conductance. These results indicate that α-EMTBL potentiates GABA responses and has properties which distinguish it from benzodiazepines or barbiturates.

Original languageEnglish
Pages (from-to)133-138
Number of pages6
JournalNeuroscience Letters
Issue number1-2
StatePublished - Apr 22 1988


  • Barbiturate
  • Benzodiazepine
  • Patch clamp
  • Picrotoxinin
  • Spinal cord neuron
  • γ-Aminobutyric acid (GABA)


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