NOVEL FORM OF LONG-TERM POTENTIATION PRODUCED BY A K+ CHANNEL BLOCKER IN THE HIPPOCAMPUS

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 (NMDA) receptor channels and maintained by the activation of CA2+-sensitive intracellular messengers2,3. We now report that in CA1, a transient block by tetraethylammonium of I(C), I(M) and the delayed rectifier (I(K)) produces a Ca2+-dependent NMDA-independent form of LTP. Our results suggest that this new form of LTP (referred as to LTP(K)) 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.