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

Abstract

LONG-term potentiation (LTP) of synaptic transmission in the hippocampus is a widely studied model of memory processes1. In the CA1 region, LTP is triggered by the entry of Ca2+ through N-methyl-D-aspartate (NMD A) receptor channels and maintained by the activation of Ca2+-sensitive intracelluar messengers2,3. 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-NMD A receptors and the consequent activation of voltage -dependent Ca2+ channels.