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There were three females and one male; mean age, 42 + 12.1 years; postmortem interval, 13.1 ± 4.7 hours. Case No. 1: female, age 75; duration of illness, 43 years (institutionalized); treatment, no neuroleptic drugs at any time, Trimeton (antihistaminic), Noludar (hypnotic), Lasix, Feosol, vitamin C; cause of death, coronary thrombosis. Case No. 2: female, age 45; duration of illness, 10 years; treatment, no indication of chronic neuroleptic treatment, chlorpromazine, 650 and 750 mg daily (orally) 2 days before death, 250 mg 4 hours before death; cause of death, suicide (jumped from high window). Case No. 3: male, age 24; duration of illness, not known but chronic; treatment, no indication of chronic neuroleptic treatment, 1100 mg of chlorpromazine (orally) within 24 hours before death; cause of death, suicide (hanging). Case No. 4: female, age 24; duration of illness, 9 years; treatment, piperacetazine, 400 mg daily until death; cause of death, suicide (jumped in front of train). Group (ii): mode-of-death controls. There were three males, all suicides; mean age, 39.7 ± 10.7 years, postmortem interval, 17.8 ± 3.9 hours. They received no antidepressant or other known drug therapy. Death was caused by CO poisoning, jumping in front of a bus, and jumping from a high window. Group (iii): normal controls. There were ten males and two females; mean age, 44.7 t 6.1 years. The ratio of young to middle aged to old was 2:1:1, same as for group (i); this ratio was maintained for brain regions for which fewer than 12 controls (subgroups of eight or four in Table 1) were analyzed. The postmortem interval was 16.5 ± 2.5 hours for the group, 16.3 ± 2.5 hours for subgroup of eight, and 13.9 ± 2.7 hours for subgroup of four. Causes of death were myocardial infarction (eight cases), accidental chest trauma (three cases), and stabbing (one case). 20. K. G. Lloyd, I. J. Farley, J. H. N. Deck, 0. Hornykiewicz, Adv. Biochem. Psychopharmacol. 11, 387 (1974). 21. I. J. Farley and 0. Hornykiewicz, in Advances in Parkinsonism, W. Birkmayer and 0. Horny*kiewicz, Eds. (Roche, Basel, 1976), p. 178. 22. J. T. Coyle and D. Henry,J. Neurochem. 21, 61 (1973); M. Palkovits, M. Brownstein, J. M. Saavedra, J. Axelrod, Brain Res. 77, 137 (1974). 23. M. Vogt, in Metabolism ofthe Nervous System, D. Richter, Ed. (Pergamon, New York, 1957), p. 553; Br. Med. Bull. 21, 57 (1965); K. F. Gey and A. Pletscher, J. Pharmacol. Exp. Ther. 133, 18 (1961); H. Ehringer, 0. Hornykiewicz, H. Lechner, Arch. Exp. Pathol. Pharmakol. 239, 507 (1960). 24. A relative increase in the density of NE terminals could result from a degeneration of the cellular elements in the affected areas with the NE terminals remaining intact. However, this possibility appears somewhat unlikely because we have evidence that other biochemical parameters, such as DA and serotonin levels, do not change in an analogous manner in the areas in question (unpublished observations). An absolute increase in the density of NE terminals could be due to several possible processes, such as faulty overdevelopment of the corresponding NE system or systems; failure of some NE terminals to regress, as part of a normal process, during postnatal development (analogous to the apparently normal decrease of the nigrostriatal DA during adolescence) [A. Carlsson and B. Winblad, J. Neural Transm. 38, 271 (1976)]; or sprouting of NE nerve endings in response to damage of some other neuronal system or systems impinging on the same perikarya [G. Raisman, Brain Res. 14, 25 (1969); R. Y. Moore, A. Bjorklund, U. Stenevi, ibid. 33, 13 (1971)]. In this latter respect, the possibility of a primary damage of the neuron system containing yaminobutyric acid is especially provoking [E. Roberts, Neurosci. Res. Program Bull. 10, 468 (1972)]. Any of these factors may confer on the afflicted brain regions the kind of special biological vulnerability that has been hypothesized as one of several possible factors predisposing the affected individual to schizophrenia [S. S. Kety, Semin. Psychiatry 4, 233 (1972); W. Pollin, Arch. Gen. Psychiatry 27, 29 (1972)]. 25. S. M. Antelman and A. R. Caggiula, Science 195, 646 (1977). 26. Supported by NIMH grant MH 20500-04 and the Clarke Institute of Psychiatry.