Novel form of long-term potentiation produced by a K+ channel blocker in the hippocampus

Nature. 1991 Jan 3;349(6304):67-9. doi: 10.1038/349067a0.


Long-term potentiation (LTP) of synaptic transmission in the hippocampus is a widely studied model of memory processes. In the CA1 region, LTP is triggered by the entry of Ca2+ through N-methyl-D-aspartate (NMDA) receptor channels and maintained by the activation of Ca2(+)-sensitive intracellular messengers. We now report that in CA1, a transient block by tetraethylammonium of IC, IM and the delayed rectifier (IK) produces a Ca2(+)-dependent NMDA-independent form of LTP. Our results suggest that this new form of LTP (referred as to LTPK) is induced by a transient enhanced release of glutamate which generates a depolarization by way of the non-NMDA receptors and the consequent activation of voltage-dependent Ca2+ channels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium Channels / drug effects*
  • Calcium Channels / physiology
  • Ibotenic Acid / analogs & derivatives*
  • Ibotenic Acid / antagonists & inhibitors
  • Ibotenic Acid / pharmacology
  • Male
  • N-Methylaspartate / antagonists & inhibitors
  • N-Methylaspartate / pharmacology*
  • Potassium Channels / drug effects*
  • Potassium Channels / physiology
  • Rats
  • Rats, Inbred Strains
  • Synapses / physiology*
  • Synaptic Transmission / drug effects*
  • Tetraethylammonium
  • Tetraethylammonium Compounds / pharmacology*
  • Time Factors
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid


  • Calcium Channels
  • Potassium Channels
  • Tetraethylammonium Compounds
  • Ibotenic Acid
  • N-Methylaspartate
  • Tetraethylammonium
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid