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This chapter summarizes studies examining the link between drugs of abuse and the behavioral neurobiology of aggressive behavior in animal models. It considers studies examining how drug abuse affects the aggressive response patterns of animals, as well as the development, activity, and function of neural systems implicated in aggression control. It shows that the effects of many commonly abused drugs, illegal and prescribed, on aggression are dependent upon the sex and species of the animal, the dosing and treatment regimen, and the behavioral testing paradigm. Although very few drugs, or drug classes, have been shown to consistently influence aggressive behavior regardless of the aforementioned factors (i.e., species, age, sex, dosing, testing paradigm), there are notable exceptions, including some anabolic androgenic steroids (AAS), nicotine, 3,4-methylenedioxymethamphetamine (MDMA), and mescaline. The administration of various types of AAS has consistently increased aggression in various animal species of varying ages regardless of experimental paradigm, whereas nicotine, MDMA, and mescaline have been shown to consistently decrease aggressive responding.
This chapter summarizes studies examining the link between drugs of abuse and the behavioral neurobiology of aggressive behavior in animal models. It considers studies examining how drug abuse affects the aggressive response patterns of animals, as well as the development, activity, and function of neural systems implicated in aggression control. It shows that the effects of many commonly abused drugs, illegal and prescribed, on aggression are dependent upon the sex and species of the animal, the dosing and treatment regimen, and the behavioral testing paradigm. Although very few drugs, or drug classes, have been shown to consistently influence aggressive behavior regardless of the aforementioned factors (i.e., species, age, sex, dosing, testing paradigm), there are notable exceptions, including some anabolic androgenic steroids (AAS), nicotine, 3,4-methylenedioxymethamphetamine (MDMA), and mescaline. The administration of various types of AAS has consistently increased aggression in various animal species of varying ages regardless of experimental paradigm, whereas nicotine, MDMA, and mescaline have been shown to consistently decrease aggressive responding.
In this second report dealing with the effects of prenatal exposure to aluminum or stress, the results of shock-elicited aggression and learned helplessness testing are presented. When compared to controls, aluminum-and stress-exposed offspring displayed significantly more aggressive responses. However, aluminum-exposed offspring spent significantly less time per aggressive response in contact with the target rod. Moreover, aluminum-exposed animals had significantly longer latencies than did stress-exposed animals during the escape-training phase of the learned helplessness study. These results indicated that the prenatal treatments employed may eventuate in behavioral effects with one of these effects being the disruption of a response inhibition/direction mechanism in the aluminum-exposed :animals.In a recent publication (Anderson, Williams, Nash, Dungan, & Davis, 1985), we demonstrated that such birth-related effects as stillbirths, aborted litters, cannibalism, and lower weights were attributable to prenatal exposure to aluminum or stress. On the other hand, several learning and/or behavior effects also have been produced by aluminum exposure. For example, Crapper and Dalton (1973) administered intracranial injections of aluminum chloride to cats and reported that the animals displayed: (1) performance decrements on delayed matching to sample tasks, and (2) poor retention of one-way avoidance responding. Similarly , Petit, Biederman, and McMullen (1980) injected aluminum tartrate into the brains of rabbits and found that treated animals required significantly more trials to learn and relearn a conditioned avoidance response . On the other hand, Bowdler et al. (1979) employed a wide variety of doses of aluminum chloride and aluminum hydroxide and then tested rat subjects on roto-rod, open-field maze, and conditionedavoidance tasks. Aluminum-treated and control groups did not differ significantlyin their retention of the conditionedavoidance task. However, it was reported that higher brain aluminum content covaried significantly with: (1) greater distances covered in the open field, and (2) less time spent on the roto rod. These data suggest that aluminum treatment may be more aptly associated with increased excitability , at least in rats. Even though the literature on the behavioral effects of prenatal stress in rats is somewhat limited, what is available appears to agree with the aluminum/activity data reported by Bowdler et al. (1979). For example, Wehmer, Porter, and Scales (1970) reported significantly more open-field behavior on the part of rats whose grandmothers were exposed to prenatal stress.The present paper reports the results of additional be- havioral tests conducted with rats prenatally exposed to aluminum or stress.' PRENATAL TREATMENTSAs previously noted (Anderson et al., 1985), 16 spermpositive female Holtsman rats were received on the second day of gestation. Six dams were exposed to a 1:4 mixture of Maalox TC and plain tap water for the remainder of gestation and constituted the alumi...
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