Abstract
In two experiments, bilateral amygdala lesions were shown to facilitate the rate of kindling from the dorsal hippocampus. This facilitation was produced equally by an amygdala lesion ipsilateral to the kindled focus, whereas a lesion contralateral to the focus was ineffective. An interesting negative correlation emerged between the kindling rate and latency to onset of forelimb clonus, i.e., the faster the kindling, the longer the convulsion latencies.
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