Article date: 1991/1/3
PubMed ID: 1845914
Journal name: Nature (ISSN: 0028-0836)
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.
Author List: Aniksztejn L, Ben-Ari Y
Publication Types: Journal Article; Research Support, Non-U.S. Gov't
Substances mentioned in the article: Calcium Channels; Potassium Channels; Tetraethylammonium Compounds; Ibotenic Acid; N-Methylaspartate; Tetraethylammonium; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;
Mesh terms: Animals; Calcium Channels/drug effects; Ibotenic Acid/analogs & derivatives; Male; N-Methylaspartate/antagonists & inhibitors; Potassium Channels/drug effects; 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;