GABAB agonists modulate a transient potassium current in cultured mammalian hippocampal neurons

Neurosci Lett. 1990 Oct 2;118(1):9-13. doi: 10.1016/0304-3940(90)90236-3.

Abstract

Depolarization of voltage-clamped cultured rat hippocampal neurons from holding potentials more negative than -60 mV produced a transient outward current with the characteristics of an A-current: it was 50% inactivated at a holding potential of -85 mV and blocked by 4-aminopyridine (1 mM). In the presence of GABA or baclofen (50-200 microM), with or without bicuculline, inactivation of this current was shifted to more positive potentials so that there was little inactivation at -70 mV. Activation of the A-current was also shifted to more positive potentials by these agonists, but the voltage dependence of activation of the sodium current was unaffected. If A-currents with similar properties can influence the time course of action potentials in presynaptic terminals. GABAB agonists could make action potentials briefer by potentiating the A-current and hence depress transmitter release.

MeSH terms

  • 4-Aminopyridine / pharmacology
  • Animals
  • Animals, Newborn / metabolism
  • Baclofen / pharmacology
  • Cells, Cultured
  • Hippocampus / drug effects
  • Hippocampus / metabolism*
  • Membrane Potentials / physiology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Potassium Channels / drug effects
  • Potassium Channels / physiology*
  • Rats
  • gamma-Aminobutyric Acid / metabolism
  • gamma-Aminobutyric Acid / physiology*

Substances

  • Potassium Channels
  • gamma-Aminobutyric Acid
  • 4-Aminopyridine
  • Baclofen