Neural systems and the inhibitory modulation of agonistic behavior: a comparison of mammalian species.
The olfactory bulb, lateral septum, medial accumbens, medial hypothalamus, dorsal and median raphe, and amygdala are known from experiments in rats to participate in the inhibitory modulation of defensiveness and predation but not social aggression. The present paper surveys the influence of these structures in the inhibitory control of these same dimensions of agonistic behavior in other species. The existing evidence suggests that lesions in the lateral septum, medial accumbens, medial hypothalamus, or the dorsal and median raphe (or PCPA-induced depletion or serotonin) induce hyperreactivity to the experimenter in mice, rats, cats, dogs, and humans in every instance where they have been tested with one exception. The exception is that lesions in the medial hypothalamus of mice do not induce heightened reactivity. The same lesions do not cause this dramatic increase in reactivity to the experimenter in gerbils, hamsters, guinea pigs, or rabbits but do heighten some other species typical patterns of defensiveness such as alarm calls and avoidance of contact with conspecifics. Lesions in these same areas in monkeys have not been observed to heighten defensive behaviors. Predatory killing or killing of young conspecifics has been observed in hamsters, mice, rats, and cats in every instance where they have been examined following lesions of the olfactory bulbs, lateral septum, medial accumbens, medial hypothalamus, or the dorsal and median raphe nuclei (or PCPA-induced depletion of serotonin). Social aggression has been decreased with these same lesions in each case where they have been examined except for septal lesions in hamsters which have been reported to heighten social aggression. Across species, the consistency with which lesions of the olfactory region, lateral septum, medial accumbens, medial hypothalamus, and dorsal and median raphe nuclei alter defensiveness and predation but not social aggression supports the inference that neural systems exist which subserve the inhibitory modulation of these dimensions of behavior. Finally, the evidence that the disruption of functioning within these structures in humans results in increased agonistic responses to environmental stimuli serves to further establish the important role of this neural circuitry in the normal inhibitory modulation of agonistic behavior in humans.
D000374:Aggression / Q000502:physiology*; D000378:Agonistic Behavior / Q000502:physiology*; D000679:Amygdala / Q000502:physiology; D000818:Animals; D001921:Brain / Q000502:physiology*; D002415:Cats; D006224:Cricetinae; D004285:Dogs; D005849:Gerbillinae; D006168:Guinea Pigs; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D008647:Mesocricetus; D051379:Mice; D009433:Neural Inhibition; D009474:Neurons / Q000502:physiology; D009714:Nucleus Accumbens / Q000502:physiology; D009830:Olfactory Bulb / Q000502:physiology; D011235:Predatory Behavior / Q000502:physiology; D011817:Rabbits; D011903:Raphe Nuclei / Q000502:physiology; D051381:Rats; D012688:Septum Pellucidum / Q000502:physiology; D012919:Social Behavior; D013045:Species Specificity