Enhancement of augmentation in the entorhinal excitatory responses during the progress of Amygdala kindling.

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Entorhinal posttetanic responses (PTRs) to 10 single (0.3Hz) stimuli immediately after train stimulus (10Hz, 100 pulses) to the amygdala were recorded from conscious rats, which had electrodes previously implanted under pentobarbital anesthesia, and the magnitude of PTRs was estimated as the area between the negative potential ascribable to excitatory activation in the averaged PTR and the baseline. When the stimulus intensity was 50-100 mA lower than threshold to induce afterdischarges (ADs), the averaged PTR showed the same magnitude as the averaged test response before train, showing no augmentation in the PTR.However, augmentation in the PTR was apparent at the intensity 25 mA lower than the AD threshold and progressively increased untill the intensity became the AD threshold. The magnitude of the averaged PTR (except for some 1-3 PTRs superimposed on ADs) was more markedly increased and showed a linear relation to the AD duration, when train stimulus with the AD threshold intensity was repeated untill the AD duration became about 30 s. The increase of PTR first occurred in the mono- and later in the polysynaptic component during the developmental stages of kindling. In the hippocampal PTRs, augmentation became to be increased more latoly than in the entorhinal cortex. An NMDA receptor antagonist (CPP) and GABA receptor agonist (pentobarbital) markedly deppressed ADs and blocked kindling seizures in association with a decrease in augmentation in PTRs. These results indicate that enhancement of augmentation based on NMDA receptor activation in the PTR is involved in the origin of development of ADs and seizures during the early course of kindling.