The Role of the Amygdala in Escape-Avoidance Behaviors

Abstract

I first became interested in the influence of the amygdala on escape-avoidance behavior several years ago when I somewhat inadvertently induced temporal lobe seizures and marked “personality changes” in cats by the administration of minute quantities of acetylcholine to the basolateral portion of the amygdaloid complex (Grossman, 1963). The injections produced epileptiform spike discharges in the amygdaloid complex which spread rapidly to other portions of the temporal lobe, and involved eventually other regions of the brain. Overt psychomotor seizures typically appeared within 10–15 minutes after the injection, and persisted with minor interruptions for several hours. Afterwards, the animals appeared exhausted, but were clearly hypersensitive to any form of external stimulation, and attacked the experimenter rather than permit normal handling. Additional brief (2–5 min) epileptiform seizure attacks were observed during the next 24–48 hours. The electroencephalographic (EEG) activity of the temporal lobe remained highly abnormal for 10–15 days after the motor disturbances had subsided, and the animals continued to attack man as well as other animals (cats and rats) at the slightest provocation.