Simultaneous expression of excitatory postsynaptic potential/spike potentiation and excitatory postsynaptic potential/spike depression in the hippocampus.

Tetanic stimulation of afferents in the stratum radiatum of the CA1 area of the rat hippocampus results in long-term potentiation of excitatory synaptic responses in pyramidal cells. Previous studies have reported a greater increase in the population spike amplitude following the induction of long-term potentiation than could be accounted for by the increase of the slope of the population excitatory postsynaptic potential. Two hypotheses have been proposed to explain this phenomenon (called excitatory postsynaptic potential/spike potentiation): a modification of the firing threshold and/or a modification of the inhibitory drive. Previous studies have not, however, addressed the question of possible changes in spike threshold in association with long-term depression. This paper examines whether the concomitant long-term potentiation of pharmacologically isolated N-methyl-D-aspartate receptor-mediated excitatory postsynaptic potentials, reported previously, is also associated with a change in spike threshold. When the amplitude of the population spike is plotted as a function of the slope of the population excitatory postsynaptic potential (excitatory postsynaptic potential/spike curve), excitatory postsynaptic potential/spike potentiation (depression) is seen as a shift of the excitatory postsynaptic potential/spike curve to the left (right) following a conditioning stimulus. In this study, using kainic acid lesioned hippocampus, we have shown that tetanic stimulation produced excitatory postsynaptic potential/spike potentiation of the control synaptic response and excitatory postsynaptic potential/spike depression of the isolated N-methyl-D-aspartate receptor-mediated responses.