An antagonistic relationship between epilepsy and psychosis has been claimed. On the other hand, abnormality of the N. accumbens is thought to be involved in schizophrenia and temporal lobe epilepsy. In order to examine the role of the N. accumbens in limbic seizure and psychosis, the following were studied: 1. Amygdaloid kindling and the functional change of the N. accumbens, 2. Accumbens kindling, 3. Functional change of limbic nuclei following the accumbens kindling, and 4. The effects of lesioning of the N. accumbens on the amygdaloid kindling. The results were as follows: 1. The amygdaloid kindling induced epileptic focus and positive transfer into the N. accumbens. 2. The kindling phenomenon was confirmed positive by repeated stimulation of the N. accumbens. Clinicoelectrographic seizure development during the N. accumbens kindling resembled that of amygdaloid kindling. The mean minimum intensities to induce afterdischarge and kindling rate were 620μA and 23days, respectively. 3. Positive transfer was found in the N. amygdala and hippocampus following the accumbens kindling. 4. Lesioning of the N. accumbens had no effect on amygdaloid seizure development, but lowered the threshold intensity to induce amygdaloid afterdischarge after kindling. It was concluded that the N. accumbens and the N. amygdala formed epileptic hyperexcitability reciprocally and that the N. accumbens had an inhibitory effect on the limbic seizure, but no effect on the developed amygdaloid kindling.