An animal model for type 2 alcoholism? Alcohol consumption and aggressive behavior following lesions in the raphe nuclei, medial hypothalamus, or ventral striatum-septal area

• Published in: Physiology & behavior Vol. 60; no. 4; pp. 1125 - 1135
• Main Authors: Bergvall, Åsa H., Fahlke, Claudia, Hansen, Stefan
• Format: Journal Article
• Language: English
• Published: Cambridge Elsevier Inc 01.10.1996; New York, NY Elsevier
• Subjects: Aggression; Aggression - psychology; Alcohol Drinking; Alcoholism; Alcoholism - physiopathology; Anatomical correlates of behavior; Animal; Animals; Behavior; Behavior, Animal - physiology; Behavioral psychophysiology; Biological and medical sciences; Disease Models; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Hyperreactivity; Hypothalamus; Hypothalamus - physiology; Male; Medial hypothalamus; physiology; physiopathology; Psychology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psykologi; Raphe Nuclei; Raphe Nuclei - physiology; Rats; Rats, Wistar; Septal Nuclei; Septal Nuclei - physiology; Ventral striatum; Wistar; Medial hypothalamus; Raphe nuclei; Ventral striatum; Alcohol drinking; Hyperreactivity; Aggression; Animal model; Ethanol; Rat; Alcoholism; Defensive behavior; Rodentia; Central nervous system; Septum; Male; Drinking; Basal ganglion; Corpus striatum; Hypothalamus; Vertebrata; Mammalia; Animal; Raphe nucleus; Lesion; Brain (vertebrata); Aggressiveness
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/0031-9384(96)00169-2

Given the conspicuous association between aggressive antisocial traits and alcoholism in men, we investigated whether or not a link between defensive aggressive behavior and homecage alcohol consumption could be demonstrated in the laboratory rat. This was accomplished by observing ethanol intake and hyperreactivity towards the experimenter in rats made hyperdefensive by brain lesions. Rats with medial hypothalamic electrocoagulations showed a remarkable degree of hyperdefensiveness, lasting throughout the entire 6-week postoperative period. Alcohol intake, on the other hand, was not different from sham-operated controls when the beverage was offered as a plain 6% solution or in a 0.2% saccharin vehicle. When subjected to the stress of food restriction, which enhances ethanol intake in normal rats, medial hypothalamic subjects actually decreased their alcohol consumption. Electrolytic lesions in the dorsal and median raphe brought about a transient increase in defensive aggression, but no alteration in ethanol drinking. Animals with ibotenic acid-induced extensive lesions to the ventral striatum and septal area were not only viciously aggressive, but also drank considerably more alcohol than controls. Ibotenic acid-lesioned rats did not respond to the saccharin or food-restriction conditions by increasing their alcohol intake further, perhaps because they drank at a maximal rate already during the plain ethanol-phase of the experiment. These observations show that basal forebrain dysfunction in the rat can give rise to excessive alcohol intake and heightened aggression, a constellation of behavioral symptoms observed in male type 2 alcoholics.