Allylisopropylacetamide (AIA), a porphyria-inducing compound, produces biochemical changes simulating those occurring in acute intermittent porphyria, an inborn error of metabolism characterized by neuropsychiatric symptoms. Little is known, however, about behavior or brain activity in experimental porphyria. Effects of AIA on performance of a discrimination task, on limbic system excitability, and on brain electroencephalographic activity were studied in cats. Small doses blocked learned reactions to environmental signals and to direct limbic system stimulation without impairing motility, sensory function, motivation, or level of arousal. Thresholds for evoking hippocampal after-discharges were markedly elevated. Additional behavioral aberrations and changes in brain electrical activity were induced by higher doses. Findings suggest that AIA decreases hippocampal excitability and interferes with ability to utilize certain signals which have acquired motivational significance during past learning experiences. This experimental model should prove helpful in studying neural and behavioral factors in the pathogenesis of acute porphyria.