NMDA receptor blockade prevents LTD, but not LTP induction by intracellular tetanization

Intracellular tetanization, the activation of a postsynaptic cell without concomitant presynaptic stimulation, was applied to layer II/III pyramidal cells in slices of rat visual cortex. In standard extracellular medium, intracellular tetanization led to LTP (21 of 43 inputs) or LTD (14 of 43 inputs), the direction of the amplitude change depending on initial paired-pulse facilitation (PPF) ratio: inputs with high initial PPF ratio were usually potentiated, and inputs with initially low PPF were most often depressed or did not change. When applied during blockade of NMDA receptors (50 microM APV), intracellular tetanization failed to induce LTD, but was still capable of inducing LTP (14 of 26 inputs). Although LTP could occur in inputs with both, low and high initial PPF ratio, the correlation between the amplitude change and initial PPF ratio remained: potentiation was stronger in inputs with initially higher PPF. These data suggest that intracellular tetanization activated simultaneously NMDA receptor-dependent LTD mechanisms and NMDA receptor-independent LTP mechanisms, the final change of synaptic gain depending on their balance.